TY - JOUR
T1 - Harnessing function of EMT in cancer drug resistance
T2 - a metastasis regulator determines chemotherapy response
AU - Ebrahimi, Nasim
AU - Manavi, Mahdokht Sadat
AU - Faghihkhorasani, Ferdos
AU - Fakhr, Siavash Seifollahy
AU - Baei, Fatemeh Jafari
AU - Khorasani, Fereshteh Faghih
AU - Zare, Mohammad Mehdi
AU - Far, Nazanin Pazhouhesh
AU - Rezaei-Tazangi, Fatemeh
AU - Ren, Jun
AU - Reiter, Russel J.
AU - Nabavi, Noushin
AU - Aref, Amir Reza
AU - Chen, Chu
AU - Ertas, Yavuz Nuri
AU - Lu, Qi
N1 - Publisher Copyright:
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.
PY - 2024/3
Y1 - 2024/3
N2 - 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.
AB - 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.
KW - Mesenchymal-to-epithelial transition (MET)
KW - Multidrug-resistance (MDR)
KW - Non-coding RNAs
KW - Signaling pathways
KW - Targeting therapy
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U2 - 10.1007/s10555-023-10162-7
DO - 10.1007/s10555-023-10162-7
M3 - Review article
C2 - 38227149
AN - SCOPUS:85182464737
SN - 0167-7659
VL - 43
SP - 457
EP - 479
JO - Cancer and Metastasis Reviews
JF - Cancer and Metastasis Reviews
IS - 1
ER -