Harnessing function of EMT in cancer drug resistance: a metastasis regulator determines chemotherapy response
Cancer and Metastasis Reviews, vol.43, no.1, pp.457-479, 2024 (SCI-Expanded, Scopus)
- Publication Type: Article / Review
- Volume: 43 Issue: 1
- Publication Date: 2024
- Doi Number: 10.1007/s10555-023-10162-7
- Journal Name: Cancer and Metastasis Reviews
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Biotechnology Research Abstracts, CAB Abstracts, EMBASE, Veterinary Science Database
- Page Numbers: pp.457-479
- Keywords: Mesenchymal-to-epithelial transition (MET), Targeting therapy, Non-coding RNAs, Signaling pathways, Multidrug-resistance (MDR)
- Erciyes University Affiliated: Yes
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.