White adipose tissue-derived factors and prostate cancer progression: mechanisms and targets for interventions

1.

Hales, C. M., Carroll, M. D., Fryar, C. D., & Ogden, C. L. (2020). Prevalence of obesity and severe obesity among adults: United States, 2017–2018. NCHS Data Brief, (360), 1–8.

2.

Nomura, A. M. (2001). Body size and prostate cancer. Epidemiologic Reviews, 23(1), 126–131.CrossRef

3.

Porter, M. P., & Stanford, J. L. (2005). Obesity and the risk of prostate cancer. Prostate, 62(4), 316–321.CrossRef

4.

Roehl, K. A., Han, M., Ramos, C. G., Antenor, J. A., & Catalona, W. J. (2004). Cancer progression and survival rates following anatomical radical retropubic prostatectomy in 3,478 consecutive patients: Long-term results. Journal of Urology, 172(3), 910–914. https://doi.org/10.1097/01.ju.0000134888.22332.bbCrossRefPubMed

5.

Pound, C. R., Partin, A. W., Eisenberger, M. A., Chan, D. W., Pearson, J. D., & Walsh, P. C. (1999). Natural history of progression after PSA elevation following radical prostatectomy. JAMA, 281(17), 1591–1597.CrossRef

6.

Flavin, R., Zadra, G., & Loda, M. (2011). Metabolic alterations and targeted therapies in prostate cancer. The Journal of Pathology, 223(2), 283–294. https://doi.org/10.1002/path.2809CrossRefPubMed

7.

Cao, Y., & Ma, J. (2011). Body mass index, prostate cancer–specific mortality, and biochemical recurrence: A systematic review and meta-analysis. Cancer Prevention Research, 4(4), 486–501. https://doi.org/10.1158/1940-6207.capr-10-0229CrossRefPubMed

8.

Freedland, S. J., Terris, M. K., Presti, J. C., Jr., Amling, C. L., Kane, C. J., Trock, B., et al. (2004). Obesity and biochemical outcome following radical prostatectomy for organ confined disease with negative surgical margins. Journal of Urology, 172(2), 520–524. https://doi.org/10.1097/01.ju.0000135302.58378.aeCrossRefPubMed

9.

Campeggi, A., Xylinas, E., Ploussard, G., Ouzaid, I., Fabre, A., Allory, Y., et al. (2012). Impact of body mass index on perioperative morbidity, oncological, and functional outcomes after extraperitoneal laparoscopic radical prostatectomy. Urology, 80(3), 576–584. https://doi.org/10.1016/j.urology.2012.04.066CrossRefPubMed

10.

Haque, R., Van Den Eeden, S. K., Wallner, L. P., Richert-Boe, K., Kallakury, B., Wang, R., et al. (2014). Association of body mass index and prostate cancer mortality. Obesity Research & Clinical Practice, 8(4), e374-381. https://doi.org/10.1016/j.orcp.2013.06.002CrossRef

11.

Joshu, C. E., Mondul, A. M., Menke, A., Meinhold, C., Han, M., Humphreys, E. B., et al. (2011). Weight gain is associated with an increased risk of prostate cancer recurrence after prostatectomy in the PSA era. Cancer Prevention Research (Philadelphia, Pa.), 4(4), 544–551. https://doi.org/10.1158/1940-6207.capr-10-0257CrossRef

12.

Whitley, B. M., Moreira, D. M., Thomas, J. A., Aronson, W. J., Terris, M. K., Presti, J. C., Jr., et al. (2011). Preoperative weight change and risk of adverse outcome following radical prostatectomy: Results from the Shared Equal Access Regional Cancer Hospital database. Prostate Cancer and Prostatic Diseases, 14(4), 361–366. https://doi.org/10.1038/pcan.2011.42CrossRefPubMed

13.

Chen, Q., Chen, T., Shi, W., Zhang, T., Zhang, W., Jin, Z., et al. (2016). Adult weight gain and risk of prostate cancer: A dose-response meta-analysis of observational studies. International Journal of Cancer, 138(4), 866–874. https://doi.org/10.1002/ijc.29846CrossRefPubMed

14.

Bonn, S. E., Wiklund, F., Sjolander, A., Szulkin, R., Stattin, P., Holmberg, E., et al. (2014). Body mass index and weight change in men with prostate cancer: Progression and mortality. Cancer Causes and Control, 25(8), 933–943. https://doi.org/10.1007/s10552-014-0393-3CrossRefPubMed

15.

Troeschel, A. N., Hartman, T. J., Jacobs, E. J., Stevens, V. L., Gansler, T., Flanders, W. D., et al. (2020). Postdiagnosis body mass index, weight change, and mortality from prostate cancer, cardiovascular disease, and all causes among survivors of nonmetastatic prostate cancer. Journal of Clinical Oncology, 38(18), 2018–2027. https://doi.org/10.1200/JCO.19.02185CrossRefPubMedPubMedCentral

16.

Allott, E. H., Masko, E. M., & Freedland, S. J. (2013). Obesity and prostate cancer: Weighing the evidence. European Urology, 63(5), 800–809. https://doi.org/10.1016/j.eururo.2012.11.013CrossRefPubMed

17.

Spitz, M. R., Strom, S. S., Yamamura, Y., Troncoso, P., Babaian, R. J., Scardino, P. T., et al. (2000). Epidemiologic determinants of clinically relevant prostate cancer. International Journal of Cancer, 89(3), 259–264.CrossRef

18.

Eheman, C., Henley, S. J., Ballard-Barbash, R., Jacobs, E. J., Schymura, M. J., Noone, A. M., et al. (2012). Annual Report to the Nation on the status of cancer, 1975–2008, featuring cancers associated with excess weight and lack of sufficient physical activity. Cancer, 118(9), 2338–2366. https://doi.org/10.1002/cncr.27514CrossRefPubMed

19.

Zadra, G., Photopoulos, C., & Loda, M. (2013). The fat side of prostate cancer. Biochimica Et Biophysica Acta-Molecular and Cell Biology of Lipids, 1831(10), 1518–1532. https://doi.org/10.1016/J.Bbalip.2013.03.010

20.

Blando, J., Saha, A., Kiguchi, K., & DiGiovanni, J. (2013). Obesity, inflammation and prostate cancer. In A. J. Dannenberg, & N. A. Berger (Eds.), Obesity, inflammation and cancer (Vol. 7, pp. 235–256, Energy Balance and Cancer, Vol. 7). Springer.

21.

De Nunzio, C., Albisinni, S., Freedland, S. J., Miano, L., Cindolo, L., Finazzi Agro, E., et al. (2013). Abdominal obesity as risk factor for prostate cancer diagnosis and high grade disease: A prospective multicenter Italian cohort study. Urologic Oncology, 31(7), 997–1002. https://doi.org/10.1016/j.urolonc.2011.08.007CrossRefPubMed

22.

van Kruijsdijk, R. C., van der Wall, E., & Visseren, F. L. (2009). Obesity and cancer: The role of dysfunctional adipose tissue. Cancer Epidemiology, Biomarkers & Prevention, 18(10), 2569–2578. https://doi.org/10.1158/1055-9965.EPI-09-0372CrossRef

23.

Lysaght, J., van der Stok, E. P., Allott, E. H., Casey, R., Donohoe, C. L., Howard, J. M., et al. (2011). Pro-inflammatory and tumour proliferative properties of excess visceral adipose tissue. Cancer Letters, 312(1), 62–72. https://doi.org/10.1016/j.canlet.2011.07.034CrossRefPubMed

24.

Coussens, L. M., & Werb, Z. (2002). Inflammation and cancer. Nature, 420(6917), 860–867. https://doi.org/10.1038/nature01322CrossRefPubMedPubMedCentral

25.

Cowey, S., & Hardy, R. W. (2006). The metabolic syndrome: A high-risk state for cancer? American Journal of Pathology, 169(5), 1505–1522. https://doi.org/10.2353/ajpath.2006.051090CrossRefPubMedPubMedCentral

26.

Park, J., Euhus, D. M., & Scherer, P. E. (2011). Paracrine and endocrine effects of adipose tissue on cancer development and progression. Endocrine Reviews, 32(4), 550–570. https://doi.org/10.1210/er.2010-0030CrossRefPubMedPubMedCentral

27.

Baillargeon, J., & Rose, D. P. (2006). Obesity, adipokines, and prostate cancer (review). International Journal of Oncology, 28(3), 737–745.PubMed

28.

Trayhurn, P., & Wood, I. S. (2004). Adipokines: Inflammation and the pleiotropic role of white adipose tissue. British Journal of Nutrition, 92(3), 347–355.CrossRef

29.

Ouchi, N., Parker, J. L., Lugus, J. J., & Walsh, K. (2011). Adipokines in inflammation and metabolic disease. Nature Reviews Immunology, 11(2), 85–97. https://doi.org/10.1038/nri2921CrossRefPubMedPubMedCentral

30.

Khandekar, M. J., Cohen, P., & Spiegelman, B. M. (2011). Molecular mechanisms of cancer development in obesity. Nature Reviews Cancer, 11(12), 886–895. https://doi.org/10.1038/nrc3174CrossRefPubMed

31.

Roberts, D. L., Dive, C., & Renehan, A. G. (2010). Biological mechanisms linking obesity and cancer risk: New perspectives. Annual Review of Medicine, 61, 301–316. https://doi.org/10.1146/annurev.med.080708.082713CrossRefPubMed

32.

Grossmann, M. E., Ray, A., Nkhata, K. J., Malakhov, D. A., Rogozina, O. P., Dogan, S., et al. (2010). Obesity and breast cancer: Status of leptin and adiponectin in pathological processes. Cancer and Metastasis Reviews, 29(4), 641–653. https://doi.org/10.1007/s10555-010-9252-1CrossRefPubMed

33.

Johnson, A. R., Milner, J. J., & Makowski, L. (2012). The inflammation highway: Metabolism accelerates inflammatory traffic in obesity. Immunological Reviews, 249(1), 218–238. https://doi.org/10.1111/j.1600-065X.2012.01151.xCrossRefPubMedPubMedCentral

34.

Weisberg, S. P., McCann, D., Desai, M., Rosenbaum, M., Leibel, R. L., & Ferrante, A. W., Jr. (2003). Obesity is associated with macrophage accumulation in adipose tissue. The Journal of Clinical Investigation, 112(12), 1796–1808. https://doi.org/10.1172/JCI19246CrossRefPubMedPubMedCentral

35.

Lengyel, E., Makowski, L., DiGiovanni, J., & Kolonin, M. G. (2018). Cancer as a matter of fat: The crosstalk between adipose tissue and tumors. Trends in Cancer, 4(5), 374–384. https://doi.org/10.1016/j.trecan.2018.03.004CrossRefPubMedPubMedCentral

36.

Laurent, V., Guerard, A., Mazerolles, C., Le Gonidec, S., Toulet, A., Nieto, L., et al. (2016). Periprostatic adipocytes act as a driving force for prostate cancer progression in obesity. [Research Support, Non-U.S. Gov’t]. Nature Communications, 7, 10230. https://doi.org/10.1038/ncomms10230

37.

Palm, W., & Thompson, C. B. (2017). Nutrient acquisition strategies of mammalian cells. Nature, 546(7657), 234–242. https://doi.org/10.1038/nature22379CrossRefPubMedPubMedCentral

38.

Ye, H., Adane, B., Khan, N., Sullivan, T., Minhajuddin, M., Gasparetto, M., et al. (2016). Leukemic stem cells evade chemotherapy by metabolic adaptation to an adipose tissue niche. Cell Stem Cell, 19(1), 23–37. https://doi.org/10.1016/j.stem.2016.06.001CrossRefPubMedPubMedCentral

39.

Ribeiro, R., Monteiro, C., Silvestre, R., Castela, A., Coutinho, H., Fraga, A., et al. (2012). Human periprostatic white adipose tissue is rich in stromal progenitor cells and a potential source of prostate tumor stroma. [Research Support, Non-U.S. Gov’t]. Experimental Biology and Medicine, 237(10), 1155–1162. https://doi.org/10.1258/ebm.2012.012131

40.

van Roermund, J. G., Hinnen, K. A., Tolman, C. J., Bol, G. H., Witjes, J. A., Bosch, J. L., et al. (2011). Periprostatic fat correlates with tumour aggressiveness in prostate cancer patients. BJU International, 107(11), 1775–1779. https://doi.org/10.1111/j.1464-410X.2010.09811.xCrossRefPubMed

41.

Toren, P., & Venkateswaran, V. (2014). Periprostatic adipose tissue and prostate cancer progression: New insights into the tumor microenvironment. Clinical Genitourinary Cancer, 12(1), 21–26. https://doi.org/10.1016/j.clgc.2013.07.013CrossRefPubMed

42.

Finley, D. S., Calvert, V. S., Inokuchi, J., Lau, A., Narula, N., Petricoin, E. F., et al. (2009). Periprostatic adipose tissue as a modulator of prostate cancer aggressiveness. Journal of Urology, 182(4), 1621–1627. https://doi.org/10.1016/j.juro.2009.06.015CrossRefPubMed

43.

Nassar, Z. D., Aref, A. T., Miladinovic, D., Mah, C. Y., Raj, G. V., Hoy, A. J., et al. (2018). Peri-prostatic adipose tissue: The metabolic microenvironment of prostate cancer. BJU International, 121(Suppl 3), 9–21. https://doi.org/10.1111/bju.14173CrossRefPubMed

44.

Walz, J., Burnett, A. L., Costello, A. J., Eastham, J. A., Graefen, M., Guillonneau, B., et al. (2010). A critical analysis of the current knowledge of surgical anatomy related to optimization of cancer control and preservation of continence and erection in candidates for radical prostatectomy. European Urology, 57(2), 179–192. https://doi.org/10.1016/j.eururo.2009.11.009CrossRefPubMed

45.

Sung, M. T., Eble, J. N., & Cheng, L. (2006). Invasion of fat justifies assignment of stage pT3a in prostatic adenocarcinoma. Pathology, 38(4), 309–311. https://doi.org/10.1080/00313020600820914CrossRefPubMed

46.

Xie, H., Li, L., Zhu, G., Dang, Q., Ma, Z., He, D., et al. (2016). Correction: Infiltrated pre-adipocytes increase prostate cancer metastasis via modulation of the miR-301a/androgen receptor (AR)/TGF-beta1/Smad/MMP9 signals. Oncotarget, 7(50), 83829–83830. https://doi.org/10.18632/oncotarget.13913CrossRefPubMedPubMedCentral

47.

Ribeiro, R., Monteiro, C., Silvestre, R., Castela, A., Coutinho, H., Fraga, A., et al. (2012). Human periprostatic white adipose tissue is rich in stromal progenitor cells and a potential source of prostate tumor stroma. Experimental Biology and Medicine (Maywood, N.J.), 237(10), 1155–1162. https://doi.org/10.1258/ebm.2012.012131CrossRef

48.

Ribeiro, R., Monteiro, C., Cunha, V., Oliveira, M. J., Freitas, M., Fraga, A., et al. (2012). Human periprostatic adipose tissue promotes prostate cancer aggressiveness in vitro. Journal of Experimental & Clinical Cancer Research, 31, 32. https://doi.org/10.1186/1756-9966-31-32CrossRef

49.

Ribeiro, R. J., Monteiro, C. P., Cunha, V. F., Azevedo, A. S., Oliveira, M. J., Monteiro, R., et al. (2012). Tumor cell-educated periprostatic adipose tissue acquires an aggressive cancer-promoting secretory profile. Cellular Physiology and Biochemistry, 29(1–2), 233–240. https://doi.org/10.1159/000337604CrossRefPubMed

50.

Takeda, K., Sowa, Y., Nishino, K., Itoh, K., & Fushiki, S. (2015). Adipose-derived stem cells promote proliferation, migration, and tube formation of lymphatic endothelial cells in vitro by secreting lymphangiogenic factors. Annals of Plastic Surgery, 74(6), 728–736. https://doi.org/10.1097/SAP.0000000000000084CrossRefPubMed

51.

Zhang, Y., Daquinag, A. C., Amaya-Manzanares, F., Sirin, O., Tseng, C., & Kolonin, M. G. (2012). Stromal progenitor cells from endogenous adipose tissue contribute to pericytes and adipocytes that populate the tumor microenvironment. Cancer Research, 72(20), 5198–5208. https://doi.org/10.1158/0008-5472.CAN-12-0294CrossRefPubMed

52.

Himbert, C., Delphan, M., Scherer, D., Bowers, L. W., Hursting, S., & Ulrich, C. M. (2017). Signals from the adipose microenvironment and the obesity-cancer link-A systematic review. Cancer Prevention Research (Philadelphia, Pa.), 10(9), 494–506. https://doi.org/10.1158/1940-6207.CAPR-16-0322CrossRef

53.

Ribeiro, R., Monteiro, C., Catalan, V., Hu, P., Cunha, V., Rodriguez, A., et al. (2012). Obesity and prostate cancer: Gene expression signature of human periprostatic adipose tissue. BMC Medicine, 10, 108. https://doi.org/10.1186/1741-7015-10-108CrossRefPubMedPubMedCentral

54.

Kolonin, M. G., Evans, K. W., Mani, S. A., & Gomer, R. H. (2012). Alternative origins of stroma in normal organs and disease. Stem Cell Res., 8(2), 312–323. https://doi.org/10.1016/j.scr.2011.11.005CrossRefPubMed

55.

Bellows, C. F., Zhang, Y., Chen, J., Frazier, M. L., & Kolonin, M. G. (2011). Circulation of progenitor cells in obese and lean colorectal cancer patients. Cancer Epidemiology, Biomarkers & Prevention, 20(11), 2461–2468.CrossRef

56.

Bellows, C. F., Zhang, Y., Simmons, P. J., Khalsa, A. S., & Kolonin, M. G. (2011). Influence of BMI on level of circulating progenitor cells. Obesity, 19(8), 1722–1726. https://doi.org/10.1038/oby.2010.347CrossRefPubMed

57.

Zhang, Y., Daquinag, A., Traktuev, D. O., Amaya, F., Simmons, P. J., March, K. L., et al. (2009). White adipose tissue cells are recruited by experimental tumors and promote cancer progression in mouse models. Cancer Research, 69(12), 5259–5266.CrossRef

58.

Klopp, A. H., Zhang, Y., Solley, T., Amaya-Manzanares, F., Marini, F., Andreeff, M., et al. (2012). Omental adipose tissue-derived stromal cells promote vascularization and growth of endometrial tumors. Clinical Cancer Research, 18(3), 771–782. https://doi.org/10.1158/1078-0432.CCR-11-1916CrossRefPubMed

59.

Sirin, O., & Kolonin, M. G. (2013). Treatment of obesity as a potential complementary approach to cancer therapy. Drug Discovery Today, 11(12), 567–573.CrossRef

60.

Zhang, T., Tseng, C., Zhang, Y., Sirin, O., Corn, P. G., Li-Ning-Tapia, E. M., et al. (2016). CXCL1 mediates obesity-associated adipose stromal cell trafficking and function in the tumour microenvironment. Nature Communications, 7, 11674. https://doi.org/10.1038/ncomms11674CrossRefPubMedPubMedCentral

61.

Peng, Y. C., Levine, C. M., Zahid, S., Wilson, E. L., & Joyner, A. L. (2013). Sonic hedgehog signals to multiple prostate stromal stem cells that replenish distinct stromal subtypes during regeneration. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t]. Proceedings of the National Academy of Sciences, 110(51), 20611–20616. https://doi.org/10.1073/pnas.1315729110

62.

Zhang, Y., & Kolonin, M. G. (2016). Cytokine signaling regulating adipose stromal cell trafficking. Adipocyte, 5(4), 369–374. https://doi.org/10.1080/21623945.2016.1220452CrossRefPubMedPubMedCentral

63.

Kaplan, J. L., Marshall, M. A., McSkimming, C. C., Harmon, D. B., Garmey, J. C., Oldham, S. N., et al. (2015). Adipocyte progenitor cells initiate monocyte chemoattractant protein-1-mediated macrophage accumulation in visceral adipose tissue. Molecular Metabolism, 4(11), 779–794. https://doi.org/10.1016/j.molmet.2015.07.010CrossRefPubMedPubMedCentral

64.

Murdoch, C., Muthana, M., Coffelt, S. B., & Lewis, C. E. (2008). The role of myeloid cells in the promotion of tumour angiogenesis. Nature Reviews Cancer, 8(8), 618–631. https://doi.org/10.1038/nrc2444CrossRefPubMed

65.

Iyengar, N. M., Brown, K. A., Zhou, X. K., Gucalp, A., Subbaramaiah, K., Giri, D. D., et al. (2017). Metabolic obesity, adipose inflammation and elevated breast aromatase in women with normal body mass index. Cancer Prevention Research, 10(4), 235–243. https://doi.org/10.1158/1940-6207.CAPR-16-0314CrossRefPubMed

66.

Hanahan, D., & Coussens, L. M. (2012). Accessories to the crime: Functions of cells recruited to the tumor microenvironment. Cancer Cell, 21(3), 309–322. https://doi.org/10.1016/j.ccr.2012.02.022CrossRefPubMed

67.

Lu, P., Weaver, V. M., & Werb, Z. (2012). The extracellular matrix: A dynamic niche in cancer progression. Journal of Cell Biology, 196(4), 395–406. https://doi.org/10.1083/jcb.201102147CrossRefPubMedPubMedCentral

68.

Park, J., Morley, T. S., Kim, M., Clegg, D. J., & Scherer, P. E. (2014). Obesity and cancer--mechanisms underlying tumour progression and recurrence. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t Research Support, U.S. Gov’t, Non-P.H.S. Review]. Nature Reviews Endocrinology, 10(8), 455–465. https://doi.org/10.1038/nrendo.2014.94

69.

Kidd, S., Spaeth, E., Watson, K., Burks, J., Lu, H., Klopp, A., et al. (2012). Origins of the tumor microenvironment: Quantitative assessment of adipose-derived and bone marrow-derived stroma. PLoS ONE, 7(2), e30563. https://doi.org/10.1371/journal.pone.0030563CrossRefPubMedPubMedCentral

70.

Orecchioni, S., Gregato, G., Martin-Padura, I., Reggiani, F., Braidotti, P., Mancuso, P., et al. (2013). Complementary populations of human adipose CD34+ progenitor cells promote growth, angiogenesis, and metastasis of breast cancer. [Research Support, Non-U.S. Gov’t]. Cancer Research, 73(19), 5880–5891. https://doi.org/10.1158/0008-5472.CAN-13-0821

71.

Rowan, B. G., Gimble, J. M., Sheng, M., Anbalagan, M., Jones, R. K., Frazier, T. P., et al. (2014). Human adipose tissue-derived stromal/stem cells promote migration and early metastasis of triple negative breast cancer xenografts. PLoS ONE, 9(2), e89595. https://doi.org/10.1371/journal.pone.0089595CrossRefPubMedPubMedCentral

72.

Martin-Padura, I., Gregato, G., Marighetti, P., Mancuso, P., Calleri, A., Corsini, C., et al. (2012). The white adipose tissue used in lipotransfer procedures is a rich reservoir of CD34+ progenitors able to promote cancer progression. Cancer Research, 72(1), 325–334. https://doi.org/10.1158/0008-5472.CAN-11-1739CrossRefPubMed

73.

Zhao, M., Dumur, C. I., Holt, S. E., Beckman, M. J., & Elmore, L. W. (2010). Multipotent adipose stromal cells and breast cancer development: Think globally, act locally. Molecular Carcinogenesis, 49(11), 923–927. https://doi.org/10.1002/mc.20675CrossRefPubMedPubMedCentral

74.

Picon-Ruiz, M., Pan, C., Drews-Elger, K., Jang, K., Besser, A. H., Zhao, D., et al. (2016). Interactions between adipocytes and breast cancer cells stimulate cytokine production and drive Src/Sox2/miR-302b-mediated malignant progression. Cancer Research, 76(2), 491–504. https://doi.org/10.1158/0008-5472.CAN-15-0927CrossRefPubMed

75.

Nowicka, A., Marini, F. C., Solley, T. N., Elizondo, P. B., Zhang, Y., Sharp, H. J., et al. (2013). Human omental-derived adipose stem cells increase ovarian cancer proliferation, migration, and chemoresistance. PLoS ONE, 8(12), e81859. https://doi.org/10.1371/journal.pone.0081859CrossRefPubMedPubMedCentral

76.

Salimian Rizi, B., Caneba, C., Nowicka, A., Nabiyar, A. W., Liu, X., Chen, K., et al. (2015). Nitric oxide mediates metabolic coupling of omentum-derived adipose stroma to ovarian and endometrial cancer cells. [Research Support, Non-U.S. Gov’t]. Cancer Research, 75(2), 456–4571. https://doi.org/10.1158/0008-5472.CAN-14-1337

77.

Duong, M. N., Cleret, A., Matera, E. L., Chettab, K., Mathe, D., Valsesia-Wittmann, S., et al. (2015). Adipose cells promote resistance of breast cancer cells to trastuzumab-mediated antibody-dependent cellular cytotoxicity. Breast Cancer Research, 17, 57–63. https://doi.org/10.1186/s13058-015-0569-0CrossRefPubMedPubMedCentral

78.

Houthuijzen, J. M., Daenen, L. G., Roodhart, J. M., & Voest, E. E. (2012). The role of mesenchymal stem cells in anti-cancer drug resistance and tumour progression. [Review]. British Journal of Cancer, 106(12), 1901–1906. https://doi.org/10.1038/bjc.2012.201CrossRefPubMedPubMedCentral

79.

Su, F., Ahn, S., Saha, A., DiGiovanni, J., & Kolonin, M. G. (2019). Adipose stromal cell targeting suppresses prostate cancer epithelial-mesenchymal transition and chemoresistance. Oncogene, 38(11), 1979–1988. https://doi.org/10.1038/s41388-018-0558-8CrossRefPubMed

80.

Giovannucci, E., & Michaud, D. (2007). The role of obesity and related metabolic disturbances in cancers of the colon, prostate, and pancreas. Gastroenterology, 132(6), 2208–2225. https://doi.org/10.1053/j.gastro.2007.03.050CrossRefPubMed

81.

Giovannucci, E., Rimm, E. B., Colditz, G. A., Stampfer, M. J., Ascherio, A., Chute, C. C., et al. (1993). A prospective study of dietary fat and risk of prostate cancer. Journal of the National Cancer Institute, 85(19), 1571–1579.CrossRef

82.

Freedland, S. J., & Aronson, W. J. (2004). Examining the relationship between obesity and prostate cancer. Revista de Urología, 6(2), 73–81.

83.

Strom, S. S., Wang, X., Pettaway, C. A., Logothetis, C. J., Yamamura, Y., Do, K. A., et al. (2005). Obesity, weight gain, and risk of biochemical failure among prostate cancer patients following prostatectomy. Clinical Cancer Research, 11(19 Pt 1), 6889–6894.CrossRef

84.

Frasca, F., Pandini, G., Sciacca, L., Pezzino, V., Squatrito, S., Belfiore, A., et al. (2008). The role of insulin receptors and IGF-I receptors in cancer and other diseases. Archives of Physiology and Biochemistry, 114(1), 23–37. https://doi.org/10.1080/13813450801969715CrossRefPubMed

85.

Blando, J., Moore, T., Hursting, S., Jiang, G., Saha, A., Beltran, L., et al. (2011). Dietary energy balance modulates prostate cancer progression in Hi-Myc mice. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t]. Cancer Prevention Research, 4(12), 2002–2014. https://doi.org/10.1158/1940-6207.CAPR-11-0182

86.

Saha, A., Ahn, S., Blando, J., Su, F., Kolonin, M. G., & DiGiovanni, J. (2017). Proinflammatory CXCL12-CXCR4/CXCR7 signaling axis drives Myc-induced prostate cancer in obese mice. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-17-0284CrossRefPubMedPubMedCentral

87.

Rossi, E. L., Khatib, S. A., Doerstling, S. S., Bowers, L. W., Pruski, M., Ford, N. A., et al. (2018). Resveratrol inhibits obesity-associated adipose tissue dysfunction and tumor growth in a mouse model of postmenopausal claudin-low breast cancer. Molecular Carcinogenesis, 57(3), 393–407. https://doi.org/10.1002/mc.22763CrossRefPubMed

88.

Checkley, L. A., Rho, O., Angel, J. M., Cho, J., Blando, J., Beltran, L., et al. (2014). Metformin inhibits skin tumor promotion in overweight and obese mice. Cancer Prevention Research (Philadelphia, Pa.), 7(1), 54–64. https://doi.org/10.1158/1940-6207.CAPR-13-0110CrossRef

89.

Moore, T., Beltran, L., Carbajal, S., Hursting, S. D., & DiGiovanni, J. (2012). Energy balance modulates mouse skin tumor promotion through altered IGF-1R and EGFR crosstalk. Cancer Prevention Research (Philadelphia, Pa.), 5(10), 1236–1246. https://doi.org/10.1158/1940-6207.CAPR-12-0234CrossRef

90.

Aiuti, A., Webb, I. J., Bleul, C., Springer, T., & Gutierrez-Ramos, J. C. (1997). The chemokine SDF-1 is a chemoattractant for human CD34+ hematopoietic progenitor cells and provides a new mechanism to explain the mobilization of CD34+ progenitors to peripheral blood. Journal of Experimental Medicine, 185(1), 111–120.CrossRef

91.

Secchiero, P., Celeghini, C., Cutroneo, G., Di Baldassarre, A., Rana, R., & Zauli, G. (2000). Differential effects of stromal derived factor-1 alpha (SDF-1 alpha) on early and late stages of human megakaryocytic development. Anatomical Record, 260(2), 141–147.CrossRef

92.

Hattermann, K., & Mentlein, R. (2013). An infernal trio: The chemokine CXCL12 and its receptors CXCR4 and CXCR7 in tumor biology. [Review]. Annals of Anatomy, 195(2), 103–110. https://doi.org/10.1016/j.aanat.2012.10.013CrossRefPubMed

93.

Conley-LaComb, M. K., Saliganan, A., Kandagatla, P., Chen, Y. Q., Cher, M. L., & Chinni, S. R. (2013). PTEN loss mediated Akt activation promotes prostate tumor growth and metastasis via CXCL12/CXCR4 signaling. Molecular Cancer, 12(1), 85. https://doi.org/10.1186/1476-4598-12-85CrossRefPubMedPubMedCentral

94.

Rivat, C., Sebaihi, S., Van Steenwinckel, J., Fouquet, S., Kitabgi, P., Pohl, M., et al. (2014). Src family kinases involved in CXCL12-induced loss of acute morphine analgesia. Brain, Behavior, and Immunity, 38, 38–52. https://doi.org/10.1016/j.bbi.2013.11.010CrossRefPubMed

95.

Sun, X., Cheng, G., Hao, M., Zheng, J., Zhou, X., Zhang, J., et al. (2010). CXCL12 / CXCR4 / CXCR7 chemokine axis and cancer progression. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t Review]. Cancer and Metastasis Reviews, 29(4), 709–722. https://doi.org/10.1007/s10555-010-9256-x

96.

Duda, D. G., Kozin, S. V., Kirkpatrick, N. D., Xu, L., Fukumura, D., & Jain, R. K. (2011). CXCL12 (SDF1alpha)-CXCR4/CXCR7 pathway inhibition: An emerging sensitizer for anticancer therapies? Clinical Cancer Research, 17(8), 2074–2080. https://doi.org/10.1158/1078-0432.CCR-10-2636CrossRefPubMedPubMedCentral

97.

Decaillot, F. M., Kazmi, M. A., Lin, Y., Ray-Saha, S., Sakmar, T. P., & Sachdev, P. (2011). CXCR7/CXCR4 heterodimer constitutively recruits beta-arrestin to enhance cell migration. Journal of Biological Chemistry, 286(37), 32188–32197. https://doi.org/10.1074/jbc.M111.277038CrossRefPubMedPubMedCentral

98.

Levoye, A., Balabanian, K., Baleux, F., Bachelerie, F., & Lagane, B. (2009). CXCR7 heterodimerizes with CXCR4 and regulates CXCL12-mediated G protein signaling. [Research Support, Non-U.S. Gov’t]. Blood, 113(24), 6085–6093. https://doi.org/10.1182/blood-2008-12-196618

99.

Luker, K. E., Gupta, M., & Luker, G. D. (2009). Imaging chemokine receptor dimerization with firefly luciferase complementation. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t]. The FASEB Journal, 23(3), 823–834. https://doi.org/10.1096/fj.08-116749

100.

Zhao, H. B., Tang, C. L., Hou, Y. L., Xue, L. R., Li, M. Q., Du, M. R., et al. (2012). CXCL12/CXCR4 axis triggers the activation of EGF receptor and ERK signaling pathway in CsA-induced proliferation of human trophoblast cells. [Clinical Trial Research Support, Non-U.S. Gov’t]. PLoS One, 7(7), e38375. https://doi.org/10.1371/journal.pone.0038375

101.

McGinn, O. J., Marinov, G., Sawan, S., & Stern, P. L. (2012). CXCL12 receptor preference, signal transduction, biological response and the expression of 5T4 oncofoetal glycoprotein. [Research Support, Non-U.S. Gov’t]. Journal of Cell Science, 125(Pt 22), 5467–5478. https://doi.org/10.1242/jcs.109488

102.

Wang, J., Shiozawa, Y., Wang, J., Wang, Y., Jung, Y., Pienta, K. J., et al. (2008). The role of CXCR7/RDC1 as a chemokine receptor for CXCL12/SDF-1 in prostate cancer. [Research Support, N.I.H., Extramural Research Support, U.S. Gov’t, Non-P.H.S.]. Journal of Biological Chemistry, 283(7), 4283–4294. https://doi.org/10.1074/jbc.M707465200

103.

Akashi, T., Koizumi, K., Tsuneyama, K., Saiki, I., Takano, Y., & Fuse, H. (2008). Chemokine receptor CXCR4 expression and prognosis in patients with metastatic prostate cancer. Cancer Science, 99(3), 539–542. https://doi.org/10.1111/j.1349-7006.2007.00712.xCrossRefPubMed

104.

Sun, Y. X., Wang, J., Shelburne, C. E., Lopatin, D. E., Chinnaiyan, A. M., Rubin, M. A., et al. (2003). Expression of CXCR4 and CXCL12 (SDF-1) in human prostate cancers (PCa) in vivo. Journal of Cellular Biochemistry, 89(3), 462–473. https://doi.org/10.1002/jcb.10522CrossRefPubMed

105.

Mochizuki, H., Matsubara, A., Teishima, J., Mutaguchi, K., Yasumoto, H., Dahiya, R., et al. (2004). Interaction of ligand-receptor system between stromal-cell-derived factor-1 and CXC chemokine receptor 4 in human prostate cancer: A possible predictor of metastasis. Biochemical and Biophysical Research Communications, 320(3), 656–663. https://doi.org/10.1016/j.bbrc.2004.06.013CrossRefPubMed

106.

Jung, S. J., Kim, C. I., Park, C. H., Chang, H. S., Kim, B. H., Choi, M. S., et al. (2011). Correlation between chemokine receptor CXCR4 expression and prognostic factors in patients with prostate cancer. Korean Journal of Urology, 52(9), 607–611. https://doi.org/10.4111/kju.2011.52.9.607CrossRefPubMedPubMedCentral

107.

Sun, Y. X., Schneider, A., Jung, Y., Wang, J., Dai, J., Wang, J., et al. (2005). Skeletal localization and neutralization of the SDF-1(CXCL12)/CXCR4 axis blocks prostate cancer metastasis and growth in osseous sites in vivo. Journal of Bone and Mineral Research, 20(2), 318–329. https://doi.org/10.1359/JBMR.041109CrossRefPubMed

108.

Cawthorn, W. P., Scheller, E. L., Learman, B. S., Parlee, S. D., Simon, B. R., Mori, H., et al. (2014). Bone marrow adipose tissue is an endocrine organ that contributes to increased circulating adiponectin during caloric restriction. Cell Metabolism, 20(2), 368–375. https://doi.org/10.1016/j.cmet.2014.06.003CrossRefPubMedPubMedCentral

109.

Devlin, M. J., Cloutier, A. M., Thomas, N. A., Panus, D. A., Lotinun, S., Pinz, I., et al. (2010). Caloric restriction leads to high marrow adiposity and low bone mass in growing mice. Journal of Bone and Mineral Research, 25(9), 2078–2088. https://doi.org/10.1002/jbmr.82CrossRefPubMedPubMedCentral

110.

Bredella, M. A., Fazeli, P. K., Miller, K. K., Misra, M., Torriani, M., Thomas, B. J., et al. (2009). Increased bone marrow fat in anorexia nervosa. Journal of Clinical Endocrinology and Metabolism, 94(6), 2129–2136. https://doi.org/10.1210/jc.2008-2532CrossRefPubMedPubMedCentral

111.

Morris, E. V., & Edwards, C. M. (2016). Bone marrow adipose tissue: A new player in cancer metastasis to bone. Frontiers in Endocrinology (Lausanne), 7, 90. https://doi.org/10.3389/fendo.2016.00090CrossRef

112.

Herroon, M. K., Rajagurubandara, E., Hardaway, A. L., Powell, K., Turchick, A., Feldmann, D., et al. (2013). Bone marrow adipocytes promote tumor growth in bone via FABP4-dependent mechanisms. Oncotarget, 4(11), 2108–2123. https://doi.org/10.18632/oncotarget.1482CrossRefPubMedPubMedCentral

113.

Templeton, Z. S., Lie, W. R., Wang, W., Rosenberg-Hasson, Y., Alluri, R. V., Tamaresis, J. S., et al. (2015). Breast cancer cell colonization of the human bone marrow adipose tissue niche. Neoplasia, 17(12), 849–861. https://doi.org/10.1016/j.neo.2015.11.005CrossRefPubMedPubMedCentral

114.

Hardaway, A. L., Herroon, M. K., Rajagurubandara, E., & Podgorski, I. (2015). Marrow adipocyte-derived CXCL1 and CXCL2 contribute to osteolysis in metastatic prostate cancer. Clinical & Experimental Metastasis, 32(4), 353–368. https://doi.org/10.1007/s10585-015-9714-5CrossRef

115.

Matsushita, Y., Chu, A. K. Y., Ono, W., Welch, J. D., & Ono, N. (2021). Intercellular interactions of an adipogenic CXCL12-expressing stromal cell subset in murine bone marrow. Journal of Bone and Mineral Research, 36(6), 1145–1158. https://doi.org/10.1002/jbmr.4282CrossRefPubMed

116.

Hebert, C. A., & Baker, J. B. (1993). Interleukin-8: A review. Cancer Investigation, 11(6), 743–750. https://doi.org/10.3109/07357909309046949CrossRefPubMed

117.

Holmes, W. E., Lee, J., Kuang, W. J., Rice, G. C., & Wood, W. I. (2009). Structure and functional expression of a human interleukin-8 receptor. Science. 1991. 253: 1278–1280. Journal of Immunology, 183(5), 2895–2897

118.

Morohashi, H., Miyawaki, T., Nomura, H., Kuno, K., Murakami, S., Matsushima, K., et al. (1995). Expression of both types of human interleukin-8 receptors on mature neutrophils, monocytes, and natural killer cells. Journal of Leukocyte Biology, 57(1), 180–187. https://doi.org/10.1002/jlb.57.1.180CrossRefPubMed

119.

Kim, S. J., Uehara, H., Karashima, T., McCarty, M., Shih, N., & Fidler, I. J. (2001). Expression of interleukin-8 correlates with angiogenesis, tumorigenicity, and metastasis of human prostate cancer cells implanted orthotopically in nude mice. Neoplasia, 3(1), 33–42. https://doi.org/10.1038/sj.neo.7900124CrossRefPubMed

120.

Miyake, M., Lawton, A., Goodison, S., Urquidi, V., & Rosser, C. J. (2014). Chemokine (C-X-C motif) ligand 1 (CXCL1) protein expression is increased in high-grade prostate cancer. Pathology, Research and Practice, 210(2), 74–78. https://doi.org/10.1016/j.prp.2013.08.013CrossRefPubMed

121.

Straczkowski, M., Dzienis-Straczkowska, S., Stepien, A., Kowalska, I., Szelachowska, M., & Kinalska, I. (2002). Plasma interleukin-8 concentrations are increased in obese subjects and related to fat mass and tumor necrosis factor-alpha system. Journal of Clinical Endocrinology and Metabolism, 87(10), 4602–4606. https://doi.org/10.1210/jc.2002-020135CrossRefPubMed

122.

Wald, O., Shapira, O. M., & Izhar, U. (2013). CXCR4/CXCL12 axis in non small cell lung cancer (NSCLC) pathologic roles and therapeutic potential. Theranostics, 3(1), 26–33. https://doi.org/10.7150/thno.4922CrossRefPubMedPubMedCentral

123.

Brat, D. J., Bellail, A. C., & Van Meir, E. G. (2005). The role of interleukin-8 and its receptors in gliomagenesis and tumoral angiogenesis. Neuro-Oncology, 7(2), 122–133. https://doi.org/10.1215/S1152851704001061CrossRefPubMedPubMedCentral

124.

Wu, D., LaRosa, G. J., & Simon, M. I. (1993). G protein-coupled signal transduction pathways for interleukin-8. Science, 261(5117), 101–103. https://doi.org/10.1126/science.8316840CrossRefPubMed

125.

Wu, Y., Wang, S., Farooq, S. M., Castelvetere, M. P., Hou, Y., Gao, J. L., et al. (2012). A chemokine receptor CXCR2 macromolecular complex regulates neutrophil functions in inflammatory diseases. Journal of Biological Chemistry, 287(8), 5744–5755. https://doi.org/10.1074/jbc.M111.315762CrossRefPubMed

126.

Fuhler, G. M., Knol, G. J., Drayer, A. L., & Vellenga, E. (2005). Impaired interleukin-8- and GROalpha-induced phosphorylation of extracellular signal-regulated kinase result in decreased migration of neutrophils from patients with myelodysplasia. Journal of Leukocyte Biology, 77(2), 257–266. https://doi.org/10.1189/jlb.0504306CrossRefPubMed

127.

Knall, C., Worthen, G. S., & Johnson, G. L. (1997). Interleukin 8-stimulated phosphatidylinositol-3-kinase activity regulates the migration of human neutrophils independent of extracellular signal-regulated kinase and p38 mitogen-activated protein kinases. Proceedings of the National Academy of Sciences, 94(7), 3052–3057. https://doi.org/10.1073/pnas.94.7.3052CrossRef

128.

Thelen, M., Uguccioni, M., & Bosiger, J. (1995). PI 3-kinase-dependent and independent chemotaxis of human neutrophil leukocytes. Biochemical and Biophysical Research Communications, 217(3), 1255–1262. https://doi.org/10.1006/bbrc.1995.2903CrossRefPubMed

129.

Waugh, D. J., & Wilson, C. (2008). The interleukin-8 pathway in cancer. Clinical Cancer Research, 14(21), 6735–6741. https://doi.org/10.1158/1078-0432.CCR-07-4843CrossRefPubMed

130.

Chavey, C., Lazennec, G., Lagarrigue, S., Clape, C., Iankova, I., Teyssier, J., et al. (2009). CXC ligand 5 is an adipose-tissue derived factor that links obesity to insulin resistance. Cell Metabolism, 9(4), 339–349. https://doi.org/10.1016/j.cmet.2009.03.002CrossRefPubMedPubMedCentral

131.

Begley, L. A., Kasina, S., Mehra, R., Adsule, S., Admon, A. J., Lonigro, R. J., et al. (2008). CXCL5 promotes prostate cancer progression. Neoplasia, 10(3), 244–254. https://doi.org/10.1593/neo.07976CrossRefPubMedPubMedCentral

132.

Qi, Y., Zhao, W., Li, M., Shao, M., Wang, J., Sui, H., et al. (2018). High C-X-C motif chemokine 5 expression is associated with malignant phenotypes of prostate cancer cells via autocrine and paracrine pathways. International Journal of Oncology, 53(1), 358–370. https://doi.org/10.3892/ijo.2018.4388CrossRefPubMed

133.

Ammirante, M., Shalapour, S., Kang, Y., Jamieson, C. A., & Karin, M. (2014). Tissue injury and hypoxia promote malignant progression of prostate cancer by inducing CXCL13 expression in tumor myofibroblasts. Proceedings of the National Academy of Sciences, 111(41), 14776–14781. https://doi.org/10.1073/pnas.1416498111CrossRef

134.

Kusuyama, J., Bandow, K., Ohnishi, T., Amir, M. S., Shima, K., Semba, I., et al. (2019). CXCL13 is a differentiation- and hypoxia-induced adipocytokine that exacerbates the inflammatory phenotype of adipocytes through PHLPP1 induction. The Biochemical Journal, 476(22), 3533–3548. https://doi.org/10.1042/BCJ20190709CrossRefPubMed

135.

Kabir, S. M., Lee, E. S., & Son, D. S. (2014). Chemokine network during adipogenesis in 3T3-L1 cells: Differential response between growth and proinflammatory factor in preadipocytes vs. adipocytes. Adipocyte, 3(2), 97–106. https://doi.org/10.4161/adip.28110CrossRefPubMedPubMedCentral

136.

El Haibi, C. P., Sharma, P. K., Singh, R., Johnson, P. R., Suttles, J., Singh, S., et al. (2010). PI3Kp110-, Src-, FAK-dependent and DOCK2-independent migration and invasion of CXCL13-stimulated prostate cancer cells. Molecular Cancer, 9, 85. https://doi.org/10.1186/1476-4598-9-85CrossRefPubMedPubMedCentral

137.

El-Haibi, C. P., Singh, R., Sharma, P. K., Singh, S., & Lillard, J. W., Jr. (2011). CXCL13 mediates prostate cancer cell proliferation through JNK signalling and invasion through ERK activation. Cell Proliferation, 44(4), 311–319. https://doi.org/10.1111/j.1365-2184.2011.00757.xCrossRefPubMedPubMedCentral

138.

El-Haibi, C. P., Sharma, P., Singh, R., Gupta, P., Taub, D. D., Singh, S., et al. (2013). Differential G protein subunit expression by prostate cancer cells and their interaction with CXCR5. Molecular Cancer, 12, 64. https://doi.org/10.1186/1476-4598-12-64CrossRefPubMedPubMedCentral

139.

Hattermann, K., Bartsch, K., Gebhardt, H. H., Mehdorn, H. M., Synowitz, M., Schmitt, A. D., et al. (2016). “Inverse signaling” of the transmembrane chemokine CXCL16 contributes to proliferative and anti-apoptotic effects in cultured human meningioma cells. Cell Communication and Signaling: CCS, 14(1), 26. https://doi.org/10.1186/s12964-016-0149-7CrossRefPubMedPubMedCentral

140.

Kurki, E., Shi, J., Martonen, E., Finckenberg, P., & Mervaala, E. (2012). Distinct effects of calorie restriction on adipose tissue cytokine and angiogenesis profiles in obese and lean mice. Nutrition & Metabolism (London), 9(1), 64. https://doi.org/10.1186/1743-7075-9-64CrossRef

141.

Jung, Y., Kim, J. K., Shiozawa, Y., Wang, J., Mishra, A., Joseph, J., et al. (2013). Recruitment of mesenchymal stem cells into prostate tumours promotes metastasis. Nature Communications, 4, 1795. https://doi.org/10.1038/ncomms2766CrossRefPubMed

142.

Kapur, N., Mir, H., Sonpavde, G. P., Jain, S., Bae, S., Lillard, J. W., Jr., et al. (2019). Prostate cancer cells hyper-activate CXCR6 signaling by cleaving CXCL16 to overcome effect of docetaxel. Cancer Letters, 454, 1–13. https://doi.org/10.1016/j.canlet.2019.04.001CrossRefPubMedPubMedCentral

143.

Kanda, H., Tateya, S., Tamori, Y., Kotani, K., Hiasa, K., Kitazawa, R., et al. (2006). MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity. The Journal of Clinical Investigation, 116(6), 1494–1505. https://doi.org/10.1172/JCI26498CrossRefPubMedPubMedCentral

144.

Sartipy, P., & Loskutoff, D. J. (2003). Monocyte chemoattractant protein 1 in obesity and insulin resistance. Proceedings of the National Academy of Sciences, 100(12), 7265–7270. https://doi.org/10.1073/pnas.1133870100CrossRef

145.

Gerhardt, C. C., Romero, I. A., Cancello, R., Camoin, L., & Strosberg, A. D. (2001). Chemokines control fat accumulation and leptin secretion by cultured human adipocytes. Molecular and Cellular Endocrinology, 175(1–2), 81–92. https://doi.org/10.1016/s0303-7207(01)00394-xCrossRefPubMed

146.

Tsaur, I., Noack, A., Makarevic, J., Oppermann, E., Waaga-Gasser, A. M., Gasser, M., et al. (2015). CCL2 chemokine as a potential biomarker for prostate cancer: A pilot study. Cancer Research and Treatment, 47(2), 306–312. https://doi.org/10.4143/crt.2014.015CrossRefPubMed

147.

Gschwandtner, M., Derler, R., & Midwood, K. S. (2019). More than just attractive: How CCL2 influences myeloid cell behavior beyond chemotaxis. Frontiers in Immunology, 10, 2759. https://doi.org/10.3389/fimmu.2019.02759CrossRefPubMedPubMedCentral

148.

Christiansen, T., Richelsen, B., & Bruun, J. M. (2005). Monocyte chemoattractant protein-1 is produced in isolated adipocytes, associated with adiposity and reduced after weight loss in morbid obese subjects. International Journal of Obesity, 29(1), 146–150. https://doi.org/10.1038/sj.ijo.0802839CrossRefPubMed

149.

Huang, M., Narita, S., Numakura, K., Tsuruta, H., Saito, M., Inoue, T., et al. (2012). A high-fat diet enhances proliferation of prostate cancer cells and activates MCP-1/CCR2 signaling. Prostate, 72(16), 1779–1788. https://doi.org/10.1002/pros.22531CrossRefPubMed

150.

Loberg, R. D., Ying, C., Craig, M., Yan, L., Snyder, L. A., & Pienta, K. J. (2007). CCL2 as an important mediator of prostate cancer growth in vivo through the regulation of macrophage infiltration. Neoplasia, 9(7), 556–562. https://doi.org/10.1593/neo.07307CrossRefPubMedPubMedCentral

151.

Mathews, J. A., Wurmbrand, A. P., Ribeiro, L., Neto, F. L., & Shore, S. A. (2014). Induction of IL-17A precedes development of airway hyperresponsiveness during diet-induced obesity and correlates with complement factor D. Frontiers in Immunology, 5, 440. https://doi.org/10.3389/fimmu.2014.00440CrossRefPubMedPubMedCentral

152.

Xu, H., Barnes, G. T., Yang, Q., Tan, G., Yang, D., Chou, C. J., et al. (2003). Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. The Journal of Clinical Investigation, 112(12), 1821–1830. https://doi.org/10.1172/JCI19451CrossRefPubMedPubMedCentral

153.

Fang, L. Y., Izumi, K., Lai, K. P., Liang, L., Li, L., Miyamoto, H., et al. (2013). Infiltrating macrophages promote prostate tumorigenesis via modulating androgen receptor-mediated CCL4-STAT3 signaling. Cancer Research, 73(18), 5633–5646. https://doi.org/10.1158/0008-5472.CAN-12-3228CrossRefPubMed

154.

Huang, R., Wang, S., Wang, N., Zheng, Y., Zhou, J., Yang, B., et al. (2020). CCL5 derived from tumor-associated macrophages promotes prostate cancer stem cells and metastasis via activating beta-catenin/STAT3 signaling. Cell Death & Disease, 11(4), 234. https://doi.org/10.1038/s41419-020-2435-yCrossRef

155.

Liu, Y., Cai, Y., Liu, L., Wu, Y., & Xiong, X. (2018). Crucial biological functions of CCL7 in cancer. PeerJ, 6, e4928. https://doi.org/10.7717/peerj.4928CrossRefPubMedPubMedCentral

156.

Van Damme, J., Proost, P., Lenaerts, J. P., & Opdenakker, G. (1992). Structural and functional identification of two human, tumor-derived monocyte chemotactic proteins (MCP-2 and MCP-3) belonging to the chemokine family. Journal of Experimental Medicine, 176(1), 59–65. https://doi.org/10.1084/jem.176.1.59CrossRefPubMed

157.

Tourniaire, F., Romier-Crouzet, B., Lee, J. H., Marcotorchino, J., Gouranton, E., Salles, J., et al. (2013). Chemokine expression in inflamed adipose tissue is mainly mediated by NF-kappaB. PLoS ONE, 8(6), e66515. https://doi.org/10.1371/journal.pone.0066515CrossRefPubMedPubMedCentral

158.

Cuesta-Gomez, N., Graham, G. J., & Campbell, J. D. M. (2021). Chemokines and their receptors: Predictors of the therapeutic potential of mesenchymal stromal cells. Journal of Translational Medicine, 19(1), 156. https://doi.org/10.1186/s12967-021-02822-5CrossRefPubMedPubMedCentral

159.

Nagarsheth, N., Wicha, M. S., & Zou, W. (2017). Chemokines in the cancer microenvironment and their relevance in cancer immunotherapy. Nature Reviews Immunology, 17(9), 559–572. https://doi.org/10.1038/nri.2017.49CrossRefPubMedPubMedCentral

160.

Ford, J., Hughson, A., Lim, K., Bardina, S. V., Lu, W., Charo, I. F., et al. (2018). CCL7 is a negative regulator of cutaneous inflammation following leishmania major infection. Frontiers in Immunology, 9, 3063. https://doi.org/10.3389/fimmu.2018.03063CrossRefPubMed

161.

Palomino, D. C., & Marti, L. C. (2015). Chemokines and immunity. Einstein (Sao Paulo), 13(3), 469–473. https://doi.org/10.1590/S1679-45082015RB3438CrossRef

162.

Zhu, F., Liu, P., Li, J., & Zhang, Y. (2014). Eotaxin-1 promotes prostate cancer cell invasion via activation of the CCR3-ERK pathway and upregulation of MMP-3 expression. Oncology Reports, 31(5), 2049–2054. https://doi.org/10.3892/or.2014.3060CrossRefPubMed

163.

Rosen, E. D., & Spiegelman, B. M. (2014). What we talk about when we talk about fat. Cell, 156(1–2), 20–44. https://doi.org/10.1016/j.cell.2013.12.012CrossRefPubMedPubMedCentral

164.

Ducharme, N. A., & Bickel, P. E. (2008). Lipid droplets in lipogenesis and lipolysis. Endocrinology, 149(3), 942–949.CrossRef

165.

Granneman, J. G., & Moore, H. P. (2008). Location, location: protein trafficking and lipolysis in adipocytes. [Research Support, N.I.H., Extramural Research Support, U.S. Gov’t, Non-P.H.S. Review]. Trends in Endocrinology & Metabolism, 19(1), 3–9. https://doi.org/10.1016/j.tem.2007.10.006

166.

Currie, E., Schulze, A., Zechner, R., Walther, T. C., & Farese, R. V., Jr. (2013). Cellular fatty acid metabolism and cancer. Cell Metabolism, 18(2), 153–161. https://doi.org/10.1016/j.cmet.2013.05.017CrossRefPubMedPubMedCentral

167.

Nomura, D. K., Lombardi, D. P., Chang, J. W., Niessen, S., Ward, A. M., Long, J. Z., et al. (2011). Monoacylglycerol lipase exerts dual control over endocannabinoid and fatty acid pathways to support prostate cancer. Chemistry & Biology, 18(7), 846–856. https://doi.org/10.1016/j.chembiol.2011.05.009CrossRef

168.

Wang, Y. Y., Attane, C., Milhas, D., Dirat, B., Dauvillier, S., Guerard, A., et al. (2017). Mammary adipocytes stimulate breast cancer invasion through metabolic remodeling of tumor cells. JCI Insight, 2(4), e87489. https://doi.org/10.1172/jci.insight.87489CrossRefPubMedPubMedCentral

169.

Arner, P., & Langin, D. (2014). Lipolysis in lipid turnover, cancer cachexia, and obesity-induced insulin resistance. Trends in Endocrinology and Metabolism, 25(5), 255–262. https://doi.org/10.1016/j.tem.2014.03.002CrossRefPubMed

170.

Rohm, M., Schafer, M., Laurent, V., Ustunel, B. E., Niopek, K., Algire, C., et al. (2016). An AMP-activated protein kinase-stabilizing peptide ameliorates adipose tissue wasting in cancer cachexia in mice. Nature Medicine, 22(10), 1120–1130. https://doi.org/10.1038/nm.4171CrossRefPubMed

171.

Okumura, T., Ohuchida, K., Sada, M., Abe, T., Endo, S., Koikawa, K., et al. (2017). Extra-pancreatic invasion induces lipolytic and fibrotic changes in the adipose microenvironment, with released fatty acids enhancing the invasiveness of pancreatic cancer cells. Oncotarget, 8(11), 18280–18295. https://doi.org/10.18632/oncotarget.15430CrossRefPubMedPubMedCentral

172.

Yamaguchi, J., Ohtani, H., Nakamura, K., Shimokawa, I., & Kanematsu, T. (2008). Prognostic impact of marginal adipose tissue invasion in ductal carcinoma of the breast. American Journal of Clinical Pathology, 130(3), 382–388. https://doi.org/10.1309/MX6KKA1UNJ1YG8VNCrossRefPubMed

173.

Nieman, K. M., Kenny, H. A., Penicka, C. V., Ladanyi, A., Buell-Gutbrod, R., Zillhardt, M. R., et al. (2011). Adipocytes promote ovarian cancer metastasis and provide energy for rapid tumor growth. Nature Medicine, 17(11), 1498–1503. https://doi.org/10.1038/nm.2492CrossRefPubMedPubMedCentral

174.

Dirat, B., Bochet, L., Dabek, M., Daviaud, D., Dauvillier, S., Majed, B., et al. (2011). Cancer-associated adipocytes exhibit an activated phenotype and contribute to breast cancer invasion. Cancer Research, 71(7), 2455–2465. https://doi.org/10.1158/0008-5472.CAN-10-3323CrossRefPubMed

175.

Balaban, S., Shearer, R. F., Lee, L. S., van Geldermalsen, M., Schreuder, M., Shtein, H. C., et al. (2017). Adipocyte lipolysis links obesity to breast cancer growth: Adipocyte-derived fatty acids drive breast cancer cell proliferation and migration. Cancer & Metabolism, 5, 1. https://doi.org/10.1186/s40170-016-0163-7CrossRef

176.

Wen, Y. A., Xing, X., Harris, J. W., Zaytseva, Y. Y., Mitov, M. I., Napier, D. L., et al. (2017). Adipocytes activate mitochondrial fatty acid oxidation and autophagy to promote tumor growth in colon cancer. Cell Death & Disease, 8(2), e2593. https://doi.org/10.1038/cddis.2017.21CrossRef

177.

Daquinag, A. C., Gao, Z., Fussell, C., Immaraj, L., Pasqualini, R., Arap, W., et al. (2021). Fatty acid mobilization from adipose tissue is mediated by CD36 posttranslational modifications and intracellular trafficking. JCI Insight, 6(17). https://doi.org/10.1172/jci.insight.147057

178.

Su, F., Daquinag, A. C., Ahn, S., Saha, A., Dai, Y., Zhao, Z., et al. (2021). Progression of prostate carcinoma is promoted by adipose stromal cell-secreted CXCL12 signaling in prostate epithelium. NPJ Precision Oncology, 5(1), 26. https://doi.org/10.1038/s41698-021-00160-9CrossRefPubMedPubMedCentral

179.

Leitner, B. P., Huang, S., Brychta, R. J., Duckworth, C. J., Baskin, A. S., McGehee, S., et al. (2017). Mapping of human brown adipose tissue in lean and obese young men. Proceedings of the National Academy of Sciences, 114(32), 8649–8654. https://doi.org/10.1073/pnas.1705287114CrossRef

180.

Alvarez-Artime, A., Garcia-Soler, B., Sainz, R. M., & Mayo, J. C. (2021). Emerging roles for browning of white adipose tissue in prostate cancer malignant behaviour. International Journal of Molecular Sciences, 22(11). https://doi.org/10.3390/ijms22115560

181.

Collins, S. (2011). beta-Adrenoceptor signaling networks in adipocytes for recruiting stored fat and energy expenditure. Frontiers in Endocrinology (Lausanne), 2, 102. https://doi.org/10.3389/fendo.2011.00102CrossRef

182.

Puigserver, P., Wu, Z., Park, C. W., Graves, R., Wright, M., & Spiegelman, B. M. (1998). A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis. Cell, 92(6), 829–839. https://doi.org/10.1016/s0092-8674(00)81410-5CrossRefPubMed

183.

Hursting, S. D., Dunlap, S. M., Ford, N. A., Hursting, M. J., & Lashinger, L. M. (2013). Calorie restriction and cancer prevention: A mechanistic perspective. Cancer & Metabolism, 1(1), 10. https://doi.org/10.1186/2049-3002-1-10CrossRef

184.

Galet, C., Gray, A., Said, J. W., Castor, B., Wan, J., Beltran, P. J., et al. (2013). Effects of calorie restriction and IGF-1 receptor blockade on the progression of 22Rv1 prostate cancer xenografts. International Journal of Molecular Sciences, 14(7), 13782–13795. https://doi.org/10.3390/ijms140713782CrossRefPubMedPubMedCentral

185.

Freedland, S. J., Mavropoulos, J., Wang, A., Darshan, M., Demark-Wahnefried, W., Aronson, W. J., et al. (2008). Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate, 68(1), 11–19. https://doi.org/10.1002/pros.20683CrossRefPubMedPubMedCentral

186.

Allott, E. H., & Hursting, S. D. (2015). Obesity and cancer: Mechanistic insights from transdisciplinary studies. Endocrine-Related Cancer, 22(6), R365-386. https://doi.org/10.1530/ERC-15-0400CrossRefPubMedPubMedCentral

187.

Dorling, J. L., van Vliet, S., Huffman, K. M., Kraus, W. E., Bhapkar, M., Pieper, C. F., et al. (2020). Effects of caloric restriction on human physiological, psychological, and behavioral outcomes: Highlights from CALERIE phase 2. Nutrition Reviews. https://doi.org/10.1093/nutrit/nuaa085CrossRefPubMedCentral

188.

Harvie, M., Wright, C., Pegington, M., McMullan, D., Mitchell, E., Martin, B., et al. (2013). The effect of intermittent energy and carbohydrate restriction v. daily energy restriction on weight loss and metabolic disease risk markers in overweight women. British Journal of Nutrition, 110(8), 1534–1547. https://doi.org/10.1017/S0007114513000792CrossRefPubMed

189.

Harvie, M. N., Pegington, M., Mattson, M. P., Frystyk, J., Dillon, B., Evans, G., et al. (2011). The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: A randomized trial in young overweight women. International Journal of Obesity, 35(5), 714–727. https://doi.org/10.1038/ijo.2010.171CrossRefPubMed

190.

Harvie, M. N., Sims, A. H., Pegington, M., Spence, K., Mitchell, A., Vaughan, A. A., et al. (2016). Intermittent energy restriction induces changes in breast gene expression and systemic metabolism. Breast Cancer Research, 18(1), 57. https://doi.org/10.1186/s13058-016-0714-4CrossRefPubMedPubMedCentral

191.

Hamilton-Reeves, J. M. (2017-2021). Weight management aimed to reduce risk and improve outcomes from radical prostatectomy (WARRIOR). (ed.). NCT03261271

192.

Dimachkie, M. D., Bechtel, M. D., Robertson, H. L., Michel, C., Lee, E. K., Sullivan, D. K., et al. (2021). Exploration of biomarkers from a pilot weight management study for men undergoing radical prostatectomy. Urologic Oncology. https://doi.org/10.1016/j.urolonc.2021.01.010CrossRefPubMedPubMedCentral

193.

Hamilton-Reeves, J. M., Johnson, C. N., Hand, L. K., Bechtel, M. D., Robertson, H. L., Michel, C., et al. (2020). Feasibility of a weight management program tailored for overweight men with localized prostate cancer - A pilot study. Nutrition and Cancer, 1–16.https://doi.org/10.1080/01635581.2020.1856890

194.

Lin, D. W., Neuhouser, M. L., Schenk, J. M., Coleman, I. M., Hawley, S., Gifford, D., et al. (2007). Low-fat, low-glycemic load diet and gene expression in human prostate epithelium: A feasibility study of using cDNA microarrays to assess the response to dietary intervention in target tissues. Cancer Epidemiology, Biomarkers & Prevention, 16(10), 2150–2154.CrossRef

195.

Henning, S. M., Galet, C., Gollapudi, K., Byrd, J. B., Liang, P., Li, Z., et al. (2018). Phase II prospective randomized trial of weight loss prior to radical prostatectomy. Prostate Cancer and Prostatic Diseases, 21(2), 212–220. https://doi.org/10.1038/s41391-017-0001-1CrossRefPubMed

196.

Demark-Wahnefried, W., Rais-Bahrami, S., Desmond, R. A., Gordetsky, J. B., Hunter, G. R., Yang, E. S., et al. (2017). Presurgical weight loss affects tumour traits and circulating biomarkers in men with prostate cancer. [Clinical Study]. British Journal of Cancer, 117, 1303. https://doi.org/10.1038/bjc.2017.303. https://www.nature.com/articles/bjc2017303#supplementary-information

197.

Fruge, A. D., Ptacek, T., Tsuruta, Y., Morrow, C. D., Azrad, M., Desmond, R. A., et al. (2018). Dietary changes impact the gut microbe composition in overweight and obese men with prostate cancer undergoing radical prostatectomy. Journal of the Academy of Nutrition and Dietetics, 118(4), 714–723 e711. https://doi.org/10.1016/j.jand.2016.10.017

198.

Wilson, R. L., Shannon, T., Calton, E., Galvao, D. A., Taaffe, D. R., Hart, N. H., et al. (2020). Efficacy of a weight loss program prior to robot assisted radical prostatectomy in overweight and obese men with prostate cancer. Surgical Oncology, 35, 182–188. https://doi.org/10.1016/j.suronc.2020.08.006CrossRefPubMed

199.

Varady, K. A. (2011). Intermittent versus daily calorie restriction: Which diet regimen is more effective for weight loss? Obesity Reviews, 12(7), e593-601. https://doi.org/10.1111/j.1467-789X.2011.00873.xCrossRefPubMed

200.

Ozkul, C., Yalinay, M., & Karakan, T. (2019). Islamic fasting leads to an increased abundance of Akkermansia muciniphila and Bacteroides fragilis group: A preliminary study on intermittent fasting. The Turkish Journal of Gastroenterology, 30(12), 1030–1035. https://doi.org/10.5152/tjg.2019.19185CrossRefPubMedPubMedCentral

201.

Guo, Y., Luo, S., Ye, Y., Yin, S., Fan, J., & Xia, M. (2020). Intermittent fasting improves cardiometabolic risk factors and alters gut microbiota in metabolic syndrome patients. Journal of Clinical Endocrinology and Metabolism. https://doi.org/10.1210/clinem/dgaa644CrossRefPubMedPubMedCentral

202.

Johnson, J. B., Summer, W., Cutler, R. G., Martin, B., Hyun, D. H., Dixit, V. D., et al. (2007). Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma. Free Radical Biology & Medicine, 42(5), 665–674. https://doi.org/10.1016/j.freeradbiomed.2006.12.005CrossRef

203.

Schwingshackl, L., Zahringer, J., Nitschke, K., Torbahn, G., Lohner, S., Kuhn, T., et al. (2020). Impact of intermittent energy restriction on anthropometric outcomes and intermediate disease markers in patients with overweight and obesity: Systematic review and meta-analyses. Critical Reviews in Food Science and Nutrition, 1–12.https://doi.org/10.1080/10408398.2020.1757616

204.

Cioffi, I., Evangelista, A., Ponzo, V., Ciccone, G., Soldati, L., Santarpia, L., et al. (2018). Intermittent versus continuous energy restriction on weight loss and cardiometabolic outcomes: A systematic review and meta-analysis of randomized controlled trials. Journal of Translational Medicine, 16(1), 371. https://doi.org/10.1186/s12967-018-1748-4CrossRefPubMedPubMedCentral

205.

Harris, L., Hamilton, S., Azevedo, L. B., Olajide, J., De Brun, C., Waller, G., et al. (2018). Intermittent fasting interventions for treatment of overweight and obesity in adults: A systematic review and meta-analysis. JBI Database of Systematic Reviews and Implementation Reports, 16(2), 507–547. https://doi.org/10.11124/JBISRIR-2016-003248CrossRefPubMed

206.

Farsijani, S., Payette, H., Morais, J. A., Shatenstein, B., Gaudreau, P., & Chevalier, S. (2017). Even mealtime distribution of protein intake is associated with greater muscle strength, but not with 3-y physical function decline, in free-living older adults: The Quebec longitudinal study on Nutrition as a Determinant of Successful Aging (NuAge study). American Journal of Clinical Nutrition, 106(1), 113–124. https://doi.org/10.3945/ajcn.116.146555CrossRefPubMed

207.

Halberg, N., Henriksen, M., Soderhamn, N., Stallknecht, B., Ploug, T., Schjerling, P., et al. (2005). Effect of intermittent fasting and refeeding on insulin action in healthy men. Journal of Applied Physiology (1985), 99(6), 2128–2136. https://doi.org/10.1152/japplphysiol.00683.2005

208.

Soeters, M. R., Sauerwein, H. P., Groener, J. E., Aerts, J. M., Ackermans, M. T., Glatz, J. F., et al. (2007). Gender-related differences in the metabolic response to fasting. Journal of Clinical Endocrinology and Metabolism, 92(9), 3646–3652. https://doi.org/10.1210/jc.2007-0552CrossRefPubMed

209.

Miller, K. N., Burhans, M. S., Clark, J. P., Howell, P. R., Polewski, M. A., DeMuth, T. M., et al. (2017). Aging and caloric restriction impact adipose tissue, adiponectin, and circulating lipids. Aging Cell, 16(3), 497–507. https://doi.org/10.1111/acel.12575CrossRefPubMedPubMedCentral

210.

Linford, N. J., Beyer, R. P., Gollahon, K., Krajcik, R. A., Malloy, V. L., Demas, V., et al. (2007). Transcriptional response to aging and caloric restriction in heart and adipose tissue. Aging Cell, 6(5), 673–688. https://doi.org/10.1111/j.1474-9726.2007.00319.xCrossRefPubMed

211.

Nisoli, E., Tonello, C., Cardile, A., Cozzi, V., Bracale, R., Tedesco, L., et al. (2005). Calorie restriction promotes mitochondrial biogenesis by inducing the expression of eNOS. Science, 310(5746), 314–317. https://doi.org/10.1126/science.1117728CrossRefPubMed

212.

Okita, N., Hayashida, Y., Kojima, Y., Fukushima, M., Yuguchi, K., Mikami, K., et al. (2012). Differential responses of white adipose tissue and brown adipose tissue to caloric restriction in rats. Mechanisms of Ageing and Development, 133(5), 255–266. https://doi.org/10.1016/j.mad.2012.02.003CrossRefPubMed

213.

Giovannini, S., Carter, C. S., Leeuwenburgh, C., Flex, A., Biscetti, F., Morgan, D., et al. (2020). Effects of aging and life-long moderate calorie restriction on IL-15 signaling in the rat white adipose tissue. European Review for Medical and Pharmacological Sciences, 24(5), 2738–2749. https://doi.org/10.26355/eurrev_202003_20547CrossRefPubMed

214.

Kobayashi, M., Fujii, N., Narita, T., & Higami, Y. (2018). SREBP-1c-dependent metabolic remodeling of white adipose tissue by caloric restriction. International Journal of Molecular Sciences, 19(11). https://doi.org/10.3390/ijms19113335

215.

Fujii, N., Uta, S., Kobayashi, M., Sato, T., Okita, N., & Higami, Y. (2019). Impact of aging and caloric restriction on fibroblast growth factor 21 signaling in rat white adipose tissue. Experimental Gerontology, 118, 55–64. https://doi.org/10.1016/j.exger.2019.01.001CrossRefPubMed

216.

Richman, E. L., Kenfield, S. A., Stampfer, M. J., Paciorek, A., Carroll, P. R., & Chan, J. M. (2011). Physical activity after diagnosis and risk of prostate cancer progression: Data from the cancer of the prostate strategic urologic research endeavor. Cancer Research, 71(11), 3889–3895. https://doi.org/10.1158/0008-5472.CAN-10-3932CrossRefPubMedPubMedCentral

217.

Kenfield, S. A., Stampfer, M. J., Giovannucci, E., & Chan, J. M. (2011). Physical activity and survival after prostate cancer diagnosis in the health professionals follow-up study. Journal of Clinical Oncology, 29(6), 726–732. https://doi.org/10.1200/JCO.2010.31.5226CrossRefPubMedPubMedCentral

218.

Bonn, S. E., Sjolander, A., Lagerros, Y. T., Wiklund, F., Stattin, P., Holmberg, E., et al. (2015). Physical activity and survival among men diagnosed with prostate cancer. Cancer Epidemiology, Biomarkers & Prevention, 24(1), 57–64. https://doi.org/10.1158/1055-9965.EPI-14-0707CrossRef

219.

Gunnell, A. S., Joyce, S., Tomlin, S., Taaffe, D. R., Cormie, P., Newton, R. U., et al. (2017). Physical activity and survival among long-term cancer survivor and non-cancer cohorts. Frontiers in Public Health, 5, 19. https://doi.org/10.3389/fpubh.2017.00019CrossRefPubMedPubMedCentral

220.

McTiernan, A. (2008). Mechanisms linking physical activity with cancer. Nature Reviews Cancer, 8(3), 205–211. https://doi.org/10.1038/nrc2325CrossRefPubMed

221.

Winters-Stone, K. M., Wood, L. J., Stoyles, S., & Dieckmann, N. F. (2018). The effects of resistance exercise on biomarkers of breast cancer prognosis: A pooled analysis of three randomized trials. Cancer Epidemiology, Biomarkers & Prevention, 27(2), 146–153. https://doi.org/10.1158/1055-9965.Epi-17-0766CrossRef

222.

Dai, J. Y., Wang, B., Wang, X., Cheng, A., Kolb, S., Stanford, J. L., et al. (2019). Vigorous physical activity is associated with lower risk of metastatic-lethal progression in prostate cancer and hypomethylation in the CRACR2A gene. Cancer Epidemiology, Biomarkers & Prevention, 28(2), 258–264. https://doi.org/10.1158/1055-9965.EPI-18-0622CrossRef

223.

Kim, J. S., Galvao, D. A., Newton, R. U., Gray, E., & Taaffe, D. R. (2021). Exercise-induced myokines and their effect on prostate cancer. Nature Reviews. Urology, 18(9), 519–542. https://doi.org/10.1038/s41585-021-00476-yCrossRefPubMed

224.

Schmid, M., Martins, H. C., Schratt, G., Kropfl, J. M., & Spengler, C. M. (2021). MiRNA126 - RGS16 - CXCL12 cascade as a potential mechanism of acute exercise-induced precursor cell mobilization. Frontiers in Physiology, 12, 780666. https://doi.org/10.3389/fphys.2021.780666CrossRefPubMedPubMedCentral

225.

Zaldivar, F., Eliakim, A., Radom-Aizik, S., Leu, S. Y., & Cooper, D. M. (2007). The effect of brief exercise on circulating CD34+ stem cells in early and late pubertal boys. Pediatric Research, 61(4), 491–495. https://doi.org/10.1203/pdr.0b013e3180332d36CrossRefPubMed

226.

Chang, E., Paterno, J., Duscher, D., Maan, Z. N., Chen, J. S., Januszyk, M., et al. (2015). Exercise induces stromal cell-derived factor-1alpha-mediated release of endothelial progenitor cells with increased vasculogenic function. Plastic and Reconstructive Surgery, 135(2), 340e–350e. https://doi.org/10.1097/PRS.0000000000000917CrossRefPubMed

227.

Niemiro, G. M., Parel, J., Beals, J., van Vliet, S., Paluska, S. A., Moore, D. R., et al. (2017). Kinetics of circulating progenitor cell mobilization during submaximal exercise. Journal of Applied Physiology (1985), 122(3), 675–682. https://doi.org/10.1152/japplphysiol.00936.2016

228.

Niemiro, G. M., Allen, J. M., Mailing, L. J., Khan, N. A., Holscher, H. D., Woods, J. A., et al. (2018). Effects of endurance exercise training on inflammatory circulating progenitor cell content in lean and obese adults. Journal of Physiology, 596(14), 2811–2822. https://doi.org/10.1113/JP276023CrossRefPubMedPubMedCentral

229.

Van Craenenbroeck, E. M., Beckers, P. J., Possemiers, N. M., Wuyts, K., Frederix, G., Hoymans, V. Y., et al. (2010). Exercise acutely reverses dysfunction of circulating angiogenic cells in chronic heart failure. European Heart Journal, 31(15), 1924–1934. https://doi.org/10.1093/eurheartj/ehq058CrossRefPubMed

230.

Van Craenenbroeck, E. M., Hoymans, V. Y., Beckers, P. J., Possemiers, N. M., Wuyts, K., Paelinck, B. P., et al. (2010). Exercise training improves function of circulating angiogenic cells in patients with chronic heart failure. Basic Research in Cardiology, 105(5), 665–676. https://doi.org/10.1007/s00395-010-0105-4CrossRefPubMed

231.

Ribeiro, F., Ribeiro, I. P., Goncalves, A. C., Alves, A. J., Melo, E., Fernandes, R., et al. (2017). Effects of resistance exercise on endothelial progenitor cell mobilization in women. Science and Reports, 7(1), 17880. https://doi.org/10.1038/s41598-017-18156-6CrossRef

232.

Ross, M. D., Malone, E. M., Simpson, R., Cranston, I., Ingram, L., Wright, G. P., et al. (2018). Lower resting and exercise-induced circulating angiogenic progenitors and angiogenic T cells in older men. American Journal of Physiology. Heart and Circulatory Physiology, 314(3), H392–H402. https://doi.org/10.1152/ajpheart.00592.2017CrossRefPubMed

233.

Wedell-Neergaard, A. S., Lang Lehrskov, L., Christensen, R. H., Legaard, G. E., Dorph, E., Larsen, M. K., et al. (2019). Exercise-induced changes in visceral adipose tissue mass are regulated by IL-6 signaling: A randomized controlled trial. Cell Metabolism, 29(4), 844–855 e843. https://doi.org/10.1016/j.cmet.2018.12.007

234.

Khosravi, N., Stoner, L., Farajivafa, V., & Hanson, E. D. (2019). Exercise training, circulating cytokine levels and immune function in cancer survivors: A meta-analysis. Brain, Behavior, and Immunity, 81, 92–104. https://doi.org/10.1016/j.bbi.2019.08.187CrossRefPubMed

235.

Rocha-Rodrigues, S., Matos, A., Afonso, J., Mendes-Ferreira, M., Abade, E., Teixeira, E., et al. (2021). Skeletal muscle-adipose tissue-tumor axis: Molecular mechanisms linking exercise training in prostate cancer. International Journal of Molecular Sciences, 22(9). https://doi.org/10.3390/ijms22094469

236.

Idorn, M., & Thor Straten, P. (2018). Chemokine receptors and exercise to tackle the inadequacy of T cell homing to the tumor site. Cells, 7(8). https://doi.org/10.3390/cells7080108

237.

Bourke, L., Smith, D., Steed, L., Hooper, R., Carter, A., Catto, J., et al. (2016). Exercise for men with prostate cancer: A systematic review and meta-analysis. European Urology, 69(4), 693–703. https://doi.org/10.1016/j.eururo.2015.10.047CrossRefPubMed

238.

Andersen, M. F., Midtgaard, J., & Bjerre, E. D. (2022). Do patients with prostate cancer benefit from exercise interventions? A systematic review and meta-analysis. International Journal of Environmental Research and Public Health, 19(2). https://doi.org/10.3390/ijerph19020972

239.

Newton, R. U., Kenfield, S. A., Hart, N. H., Chan, J. M., Courneya, K. S., Catto, J., et al. (2018). Intense Exercise for Survival among Men with Metastatic Castrate-Resistant Prostate Cancer (INTERVAL-GAP4): A multicentre, randomised, controlled phase III study protocol. British Medical Journal Open, 8(5), e022899. https://doi.org/10.1136/bmjopen-2018-022899CrossRef

240.

Kim, J. S., Taaffe, D. R., Galvao, D. A., Hart, N. H., Gray, E., Ryan, C. J., et al. (2022). Exercise in advanced prostate cancer elevates myokine levels and suppresses in-vitro cell growth. Prostate Cancer and Prostatic Diseases, 25(1), 86–92. https://doi.org/10.1038/s41391-022-00504-xCrossRefPubMedPubMedCentral

241.

Ingram, D. K., Zhu, M., Mamczarz, J., Zou, S., Lane, M. A., Roth, G. S., et al. (2006). Calorie restriction mimetics: An emerging research field. Aging Cell, 5(2), 97–108. https://doi.org/10.1111/j.1474-9726.2006.00202.xCrossRefPubMed

242.

Salehi, B., Mishra, A. P., Nigam, M., Sener, B., Kilic, M., Sharifi-Rad, M., et al. (2018). Resveratrol: A double-edged sword in health benefits. Biomedicines, 6(3). https://doi.org/10.3390/biomedicines6030091

243.

Lagouge, M., Argmann, C., Gerhart-Hines, Z., Meziane, H., Lerin, C., Daussin, F., et al. (2006). Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. Cell, 127(6), 1109–1122. https://doi.org/10.1016/j.cell.2006.11.013CrossRefPubMed

244.

Alberdi, G., Rodriguez, V. M., Miranda, J., Macarulla, M. T., Arias, N., Andres-Lacueva, C., et al. (2011). Changes in white adipose tissue metabolism induced by resveratrol in rats. Nutrition & Metabolism (London), 8(1), 29. https://doi.org/10.1186/1743-7075-8-29CrossRef

245.

Cho, S. J., Jung, U. J., & Choi, M. S. (2012). Differential effects of low-dose resveratrol on adiposity and hepatic steatosis in diet-induced obese mice. British Journal of Nutrition, 108(12), 2166–2175. https://doi.org/10.1017/S0007114512000347CrossRefPubMed

246.

Qiao, Y., Sun, J., Xia, S., Tang, X., Shi, Y., & Le, G. (2014). Effects of resveratrol on gut microbiota and fat storage in a mouse model with high-fat-induced obesity. Food & Function, 5(6), 1241–1249. https://doi.org/10.1039/c3fo60630aCrossRef

247.

Mendez-del Villar, M., Gonzalez-Ortiz, M., Martinez-Abundis, E., Perez-Rubio, K. G., & Lizarraga-Valdez, R. (2014). Effect of resveratrol administration on metabolic syndrome, insulin sensitivity, and insulin secretion. Metabolic Syndrome and Related Disorders, 12(10), 497–501. https://doi.org/10.1089/met.2014.0082CrossRefPubMed

248.

Arzola-Paniagua, M. A., Garcia-Salgado Lopez, E. R., Calvo-Vargas, C. G., & Guevara-Cruz, M. (2016). Efficacy of an orlistat-resveratrol combination for weight loss in subjects with obesity: A randomized controlled trial. Obesity (Silver Spring), 24(7), 1454–1463. https://doi.org/10.1002/oby.21523CrossRef

249.

Faghihzadeh, F., Adibi, P., Rafiei, R., & Hekmatdoost, A. (2014). Resveratrol supplementation improves inflammatory biomarkers in patients with nonalcoholic fatty liver disease. Nutrition Research, 34(10), 837–843. https://doi.org/10.1016/j.nutres.2014.09.005CrossRefPubMed

250.

Most, J., Timmers, S., Warnke, I., Jocken, J. W., van Boekschoten, M., de Groot, P., et al. (2016). Combined epigallocatechin-3-gallate and resveratrol supplementation for 12 wk increases mitochondrial capacity and fat oxidation, but not insulin sensitivity, in obese humans: A randomized controlled trial. American Journal of Clinical Nutrition, 104(1), 215–227. https://doi.org/10.3945/ajcn.115.122937CrossRefPubMed

251.

Sheth, S., Jajoo, S., Kaur, T., Mukherjea, D., Sheehan, K., Rybak, L. P., et al. (2012). Resveratrol reduces prostate cancer growth and metastasis by inhibiting the Akt/MicroRNA-21 pathway. PLoS ONE, 7(12), e51655. https://doi.org/10.1371/journal.pone.0051655CrossRefPubMedPubMedCentral

252.

Gill, C., Walsh, S. E., Morrissey, C., Fitzpatrick, J. M., & Watson, R. W. (2007). Resveratrol sensitizes androgen independent prostate cancer cells to death-receptor mediated apoptosis through multiple mechanisms. Prostate, 67(15), 1641–1653. https://doi.org/10.1002/pros.20653CrossRefPubMed

253.

Tan, L., Wang, W., He, G., Kuick, R. D., Gossner, G., Kueck, A. S., et al. (2016). Resveratrol inhibits ovarian tumor growth in an in vivo mouse model. Cancer, 122(5), 722–729. https://doi.org/10.1002/cncr.29793CrossRefPubMed

254.

Li, W., Ma, J., Ma, Q., Li, B., Han, L., Liu, J., et al. (2013). Resveratrol inhibits the epithelial-mesenchymal transition of pancreatic cancer cells via suppression of the PI-3K/Akt/NF-kappaB pathway. Current Medicinal Chemistry, 20(33), 4185–4194. https://doi.org/10.2174/09298673113209990251CrossRefPubMedPubMedCentral

255.

Liang, Z. J., Wan, Y., Zhu, D. D., Wang, M. X., Jiang, H. M., Huang, D. L., et al. (2021). Resveratrol mediates the apoptosis of triple negative breast cancer cells by reducing POLD1 expression. Frontiers in Oncology, 11, 569295. https://doi.org/10.3389/fonc.2021.569295CrossRefPubMedPubMedCentral

256.

Harper, C. E., Patel, B. B., Wang, J., Arabshahi, A., Eltoum, I. A., & Lamartiniere, C. A. (2007). Resveratrol suppresses prostate cancer progression in transgenic mice. Carcinogenesis, 28(9), 1946–1953. https://doi.org/10.1093/carcin/bgm144CrossRefPubMed

257.

Wang, K., Chen, Z., Shi, J., Feng, Y., Yu, M., Sun, Y., et al. (2020). Resveratrol inhibits the tumor migration and invasion by upregulating TET1 and reducing TIMP2/3 methylation in prostate carcinoma cells. Prostate, 80(12), 977–985. https://doi.org/10.1002/pros.24029CrossRefPubMed

258.

Weisberg, S. P., Leibel, R., & Tortoriello, D. V. (2008). Dietary curcumin significantly improves obesity-associated inflammation and diabetes in mouse models of diabesity. Endocrinology, 149(7), 3549–3558. https://doi.org/10.1210/en.2008-0262CrossRefPubMedPubMedCentral

259.

Shao, W., Yu, Z., Chiang, Y., Yang, Y., Chai, T., Foltz, W., et al. (2012). Curcumin prevents high fat diet induced insulin resistance and obesity via attenuating lipogenesis in liver and inflammatory pathway in adipocytes. PLoS ONE, 7(1), e28784. https://doi.org/10.1371/journal.pone.0028784CrossRefPubMedPubMedCentral

260.

Ejaz, A., Wu, D., Kwan, P., & Meydani, M. (2009). Curcumin inhibits adipogenesis in 3T3-L1 adipocytes and angiogenesis and obesity in C57/BL mice. Journal of Nutrition, 139(5), 919–925. https://doi.org/10.3945/jn.108.100966CrossRefPubMed

261.

Aggarwal, B. B., Kumar, A., & Bharti, A. C. (2003). Anticancer potential of curcumin: Preclinical and clinical studies. Anticancer Research, 23(1A), 363–398.PubMed

262.

Vafadar, A., Shabaninejad, Z., Movahedpour, A., Fallahi, F., Taghavipour, M., Ghasemi, Y., et al. (2020). Quercetin and cancer: New insights into its therapeutic effects on ovarian cancer cells. Cell & Bioscience, 10, 32. https://doi.org/10.1186/s13578-020-00397-0CrossRef

263.

Rivera, L., Moron, R., Sanchez, M., Zarzuelo, A., & Galisteo, M. (2008). Quercetin ameliorates metabolic syndrome and improves the inflammatory status in obese Zucker rats. Obesity (Silver Spring), 16(9), 2081–2087. https://doi.org/10.1038/oby.2008.315CrossRef

264.

Stewart, L. K., Soileau, J. L., Ribnicky, D., Wang, Z. Q., Raskin, I., Poulev, A., et al. (2008). Quercetin transiently increases energy expenditure but persistently decreases circulating markers of inflammation in C57BL/6J mice fed a high-fat diet. Metabolism, 57(7 Suppl 1), S39-46. https://doi.org/10.1016/j.metabol.2008.03.003CrossRefPubMedPubMedCentral

265.

Dong, J., Zhang, X., Zhang, L., Bian, H. X., Xu, N., Bao, B., et al. (2014). Quercetin reduces obesity-associated ATM infiltration and inflammation in mice: A mechanism including AMPKalpha1/SIRT1. Journal of Lipid Research, 55(3), 363–374. https://doi.org/10.1194/jlr.M038786CrossRefPubMedPubMedCentral

266.

He, Y., Cao, X., Guo, P., Li, X., Shang, H., Liu, J., et al. (2017). Quercetin induces autophagy via FOXO1-dependent pathways and autophagy suppression enhances quercetin-induced apoptosis in PASMCs in hypoxia. Free Radical Biology & Medicine, 103, 165–176. https://doi.org/10.1016/j.freeradbiomed.2016.12.016CrossRef

267.

Chondrogianni, N., Kapeta, S., Chinou, I., Vassilatou, K., Papassideri, I., & Gonos, E. S. (2010). Anti-ageing and rejuvenating effects of quercetin. Experimental Gerontology, 45(10), 763–771. https://doi.org/10.1016/j.exger.2010.07.001CrossRefPubMed

268.

Hoek-van den Hil, E. F., van Schothorst, E. M., van der Stelt, I., Swarts, H. J., Venema, D., Sailer, M., et al. (2014). Quercetin decreases high-fat diet induced body weight gain and accumulation of hepatic and circulating lipids in mice. Genes & Nutrition, 9(5), 418. https://doi.org/10.1007/s12263-014-0418-2CrossRef

269.

Mahini, H., Ainsworth, G., & Garelnabi, M. (2014). Exercise and quercetin intake reduces body weight in c57bl6 mice. Atherosclerosis, 235(2), e109–e110.CrossRef

270.

Pei, Y., Parks, J. S., & Kang, H. W. (2021). Quercetin alleviates high-fat diet-induced inflammation in brown adipose tissue. Journal of Functional Foods, 85.https://doi.org/10.1016/j.jff.2021.104614

271.

Lee, J. S., Cha, Y. J., Lee, K. H., & Yim, J. E. (2016). Onion peel extract reduces the percentage of body fat in overweight and obese subjects: A 12-week, randomized, double-blind, placebo-controlled study. Nursing Research & Practice, 10(2), 175–181. https://doi.org/10.4162/nrp.2016.10.2.175CrossRef

272.

Pfeuffer, M., Auinger, A., Bley, U., Kraus-Stojanowic, I., Laue, C., Winkler, P., et al. (2013). Effect of quercetin on traits of the metabolic syndrome, endothelial function and inflammation in men with different APOE isoforms. Nutrition, Metabolism, and Cardiovascular Diseases, 23(5), 403–409. https://doi.org/10.1016/j.numecd.2011.08.010CrossRefPubMed

273.

Martin-Montalvo, A., Mercken, E. M., Mitchell, S. J., Palacios, H. H., Mote, P. L., Scheibye-Knudsen, M., et al. (2013). Metformin improves healthspan and lifespan in mice. Nature Communications, 4, 2192. https://doi.org/10.1038/ncomms3192CrossRefPubMed

274.

Anisimov, V. N., Berstein, L. M., Egormin, P. A., Piskunova, T. S., Popovich, I. G., Zabezhinski, M. A., et al. (2008). Metformin slows down aging and extends life span of female SHR mice. Cell Cycle, 7(17), 2769–2773. https://doi.org/10.4161/cc.7.17.6625CrossRefPubMed

275.

Saha, A., Blando, J., Tremmel, L., & DiGiovanni, J. (2015). Effect of metformin, rapamycin and their combination on growth and progression of prostate tumors in himyc mice. Cancer Prevention Research (Philadelphia, Pa.). https://doi.org/10.1158/1940-6207.CAPR-15-0014CrossRef

276.

Goodwin, P. J., & Stambolic, V. (2011). Obesity and insulin resistance in breast cancer–chemoprevention strategies with a focus on metformin. Breast, 20(Suppl 3), S31-35. https://doi.org/10.1016/S0960-9776(11)70291-0CrossRefPubMed

277.

Berstein, L. M. (2012). Metformin in obesity, cancer and aging: Addressing controversies. Aging (Albany NY), 4(5), 320–329. https://doi.org/10.18632/aging.100455CrossRef

278.

Harrison, D. E., Strong, R., Sharp, Z. D., Nelson, J. F., Astle, C. M., Flurkey, K., et al. (2009). Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature, 460(7253), 392–395. https://doi.org/10.1038/nature08221CrossRefPubMedPubMedCentral

279.

Chang, G. R., Chiu, Y. S., Wu, Y. Y., Chen, W. Y., Liao, J. W., Chao, T. H., et al. (2009). Rapamycin protects against high fat diet-induced obesity in C57BL/6J mice. Journal of Pharmacological Sciences, 109(4), 496–503. https://doi.org/10.1254/jphs.08215FPCrossRefPubMed

280.

Checkley, L. A., Rho, O., Moore, T., Hursting, S., & DiGiovanni, J. (2011). Rapamycin is a potent inhibitor of skin tumor promotion by 12-O-tetradecanoylphorbol-13-acetate. Cancer Prevention Research (Philadelphia, Pa.), 4(7), 1011–1020. https://doi.org/10.1158/1940-6207.CAPR-10-0375CrossRef

281.

Lee, D., Lee, J. H., Kim, B. H., Lee, S., Kim, D. W., & Kang, K. S. (2022). Phytochemical combination (p-synephrine, p-octopamine hydrochloride, and hispidulin) for improving obesity in obese mice induced by high-fat diet. Nutrients, 14(10). https://doi.org/10.3390/nu14102164

282.

Lodi, A., Saha, A., Lu, X., Wang, B., Sentandreu, E., Collins, M., et al. (2017). Combinatorial treatment with natural compounds in prostate cancer inhibits prostate tumor growth and leads to key modulations of cancer cell metabolism. NPJ Precision Oncology, 1.https://doi.org/10.1038/s41698-017-0024-z

283.

Daquinag, A. C., Dadbin, A., Snyder, B., Wang, X., Sahin, A., Ueno, N. T., et al. (2017). Non-glycanated decorin is a drug target on human adipose stromal cells. Molecular Therapy - Oncolytics, 6, 1–9.CrossRef

284.

Daquinag, A. C., Tseng, C., Zhang, Y., Amaya-Manzanares, F., Florez, F., Dadbin, A., et al. (2016). Targeted pro-apoptotic peptides depleting adipose stromal cells inhibit tumor growth. Molecular Therapy, 1, 34–40. https://doi.org/10.1038/mt.2015.155CrossRef

285.

Daquinag, A. C., Salameh, A., Zhang, Y., Tong, Q., & Kolonin, M. G. (2015). Depletion of white adipocyte progenitors induces beige adipocyte differentiation and suppresses obesity development. Cell Death & Diff., 22, 351–363. https://doi.org/10.1038/cdd.2014.148CrossRef

286.

Zaidi, N., Lupien, L., Kuemmerle, N. B., Kinlaw, W. B., Swinnen, J. V., & Smans, K. (2013). Lipogenesis and lipolysis: The pathways exploited by the cancer cells to acquire fatty acids. Progress in Lipid Research, 52(4), 585–589. https://doi.org/10.1016/j.plipres.2013.08.005CrossRefPubMedPubMedCentral

287.

Ros, S., Santos, C. R., Moco, S., Baenke, F., Kelly, G., Howell, M., et al. (2012). Functional metabolic screen identifies 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 as an important regulator of prostate cancer cell survival. Cancer Discovery, 2(4), 328–343. https://doi.org/10.1158/2159-8290.CD-11-0234CrossRefPubMed

288.

Kuemmerle, N. B., Rysman, E., Lombardo, P. S., Flanagan, A. J., Lipe, B. C., Wells, W. A., et al. (2011). Lipoprotein lipase links dietary fat to solid tumor cell proliferation. Molecular Cancer Therapeutics, 10(3), 427–436. https://doi.org/10.1158/1535-7163.MCT-10-0802CrossRefPubMedPubMedCentral

289.

Domanska, U. M., Kruizinga, R. C., Nagengast, W. B., Timmer-Bosscha, H., Huls, G., de Vries, E. G., et al. (2013). A review on CXCR4/CXCL12 axis in oncology: No place to hide. European Journal of Cancer, 49(1), 219–230. https://doi.org/10.1016/j.ejca.2012.05.005CrossRefPubMed

290.

Zhao, H., Guo, L., Zhao, H., Zhao, J., Weng, H., & Zhao, B. (2015). CXCR4 over-expression and survival in cancer: A system review and meta-analysis. Oncotarget, 6(7), 5022–5040. https://doi.org/10.18632/oncotarget.3217CrossRefPubMed

291.

Darash-Yahana, M., Pikarsky, E., Abramovitch, R., Zeira, E., Pal, B., Karplus, R., et al. (2004). Role of high expression levels of CXCR4 in tumor growth, vascularization, and metastasis. The FASEB Journal, 18(11), 1240–1242. https://doi.org/10.1096/fj.03-0935fjeCrossRefPubMed

292.

Cui, K., Zhao, W., Wang, C., Wang, A., Zhang, B., Zhou, W., et al. (2011). The CXCR4-CXCL12 pathway facilitates the progression of pancreatic cancer via induction of angiogenesis and lymphangiogenesis. [Research Support, Non-U.S. Gov’t]. Journal of Surgical Research, 171(1), 143–150. https://doi.org/10.1016/j.jss.2010.03.001

293.

Teicher, B. A., & Fricker, S. P. (2010). CXCL12 (SDF-1)/CXCR4 pathway in cancer. Clinical Cancer Research, 16(11), 2927–2931. https://doi.org/10.1158/1078-0432.CCR-09-2329CrossRefPubMed

294.

Scala, S. (2015). Molecular pathways: Targeting the CXCR4-CXCL12 axis–Untapped potential in the tumor microenvironment. Clinical Cancer Research, 21(19), 4278–4285. https://doi.org/10.1158/1078-0432.CCR-14-0914CrossRefPubMed

295.

Bleul, C. C., Fuhlbrigge, R. C., Casasnovas, J. M., Aiuti, A., & Springer, T. A. (1996). A highly efficacious lymphocyte chemoattractant, stromal cell-derived factor 1 (SDF-1). Journal of Experimental Medicine, 184(3), 1101–1109. https://doi.org/10.1084/jem.184.3.1101CrossRefPubMed

296.

Hernandez, L., Magalhaes, M. A., Coniglio, S. J., Condeelis, J. S., & Segall, J. E. (2011). Opposing roles of CXCR4 and CXCR7 in breast cancer metastasis. Breast Cancer Research, 13(6), R128. https://doi.org/10.1186/bcr3074CrossRefPubMedPubMedCentral

297.

Ahn, S., Saha, A., Kolonin, M. G., J. DiGiovanni, J. (2021). Signaling via both CXCR4 and CXCR7 in prostate cancer cells promotes tumor progression and underlies obesity-associated epithelial-mesenchymal transition. In revision

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