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Harnessing Function of Emt in Cancer Drug Resistance: A Metastasis Regulator Determines Chemotherapy Response Publisher Pubmed



Ebrahimi N1 ; Manavi MS2 ; Faghihkhorasani F3 ; Fakhr SS4 ; Baei FJ5 ; Khorasani FF6 ; Zare MM6 ; Far NP7 ; Rezaeitazangi F8 ; Ren J9 ; Reiter RJ10 ; Nabavi N11 ; Aref AR12, 13 ; Chen C14 Show All Authors
Authors
  1. Ebrahimi N1
  2. Manavi MS2
  3. Faghihkhorasani F3
  4. Fakhr SS4
  5. Baei FJ5
  6. Khorasani FF6
  7. Zare MM6
  8. Far NP7
  9. Rezaeitazangi F8
  10. Ren J9
  11. Reiter RJ10
  12. Nabavi N11
  13. Aref AR12, 13
  14. Chen C14
  15. Ertas YN15, 16
  16. Lu Q14

Source: Cancer and Metastasis Reviews Published:2024


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. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.
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