Erschienen in:
16.01.2024 | REVIEW
Harnessing function of EMT in cancer drug resistance: a metastasis regulator determines chemotherapy response
verfasst von:
Nasim Ebrahimi, Mahdokht Sadat Manavi, Ferdos Faghihkhorasani, Siavash Seifollahy Fakhr, Fatemeh Jafari Baei, Fereshteh Faghih Khorasani, Mohammad Mehdi Zare, Nazanin Pazhouhesh Far, Fatemeh Rezaei-Tazangi, Jun Ren, Russel J. Reiter, Noushin Nabavi, Amir Reza Aref, Chu Chen, Yavuz Nuri Ertas, Qi Lu
Erschienen in:
Cancer and Metastasis Reviews
|
Ausgabe 1/2024
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Abstract
Epithelial-mesenchymal transition (EMT) is a complicated molecular process that governs cellular shape and function changes throughout tissue development and embryogenesis. In addition, EMT contributes to the development and spread of tumors. Expanding and degrading the surrounding microenvironment, cells undergoing EMT move away from the main location. On the basis of the expression of fibroblast-specific protein-1 (FSP1), fibroblast growth factor (FGF), collagen, and smooth muscle actin (-SMA), the mesenchymal phenotype exhibited in fibroblasts is crucial for promoting EMT. While EMT is not entirely reliant on its regulators like ZEB1/2, Twist, and Snail proteins, investigation of upstream signaling (like EGF, TGF-β, Wnt) is required to get a more thorough understanding of tumor EMT. Throughout numerous cancers, connections between tumor epithelial and fibroblast cells that influence tumor growth have been found. The significance of cellular crosstalk stems from the fact that these events affect therapeutic response and disease prognosis. This study examines how classical EMT signals emanating from various cancer cells interfere to tumor metastasis, treatment resistance, and tumor recurrence.