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Role of EMT in the DNA damage response, double-strand break repair pathway choice and its implications in cancer treatment

期刊

CANCER SCIENCE
卷 113, 期 7, 页码 2214-2223

出版社

WILEY
DOI: 10.1111/cas.15389

关键词

DNA damage response; DNA repair; epithelial-mesenchymal transition; synthetic lethality; ZEB1

类别

资金

  1. Ligue contre le Cancer [EL2016]
  2. LNCC/AIP [ANR--17--CONV--0002, ANR--10--LABX--0061]
  3. JSPS KAKENHI [20K21555, 20H04789, AMED P--CREATE (21cm0106184h0001)]
  4. Nippon Foundation
  5. Agence Nationale de la Recherche (ANR) [ANR-17-CONV-0002] Funding Source: Agence Nationale de la Recherche (ANR)
  6. Grants-in-Aid for Scientific Research [20H04789, 20K21555] Funding Source: KAKEN

向作者/读者索取更多资源

EMT is involved in tumor development and DNA repair. Understanding the role of EMT in DNA repair can lead to new treatments targeting tumors and improving efficacy.
Numerous epithelial-mesenchymal transition (EMT) characteristics have now been demonstrated to participate in tumor development. Indeed, EMT is involved in invasion, acquisition of stem cell properties, and therapy-associated resistance of cancer cells. Together, these mechanisms offer advantages in adapting to changes in the tumor microenvironment. However, recent findings have shown that EMT-associated transcription factors (EMT-TFs) may also be involved in DNA repair. A better understanding of the coordination between the DNA repair pathways and the role played by some EMT-TFs in the DNA damage response (DDR) should pave the way for new treatments targeting tumor-specific molecular vulnerabilities, which result in selective destruction of cancer cells. Here we review recent advances, providing novel insights into the role of EMT in the DDR and repair pathways, with a particular focus on the influence of EMT on cellular sensitivity to damage, as well as the implications of these relationships for improving the efficacy of cancer treatments.

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