Open AccessRole of EMT in the DNA damage response, double‐strand break repair pathway choice and its implications in cancer treatment
Author(s) -
MoyretLalle Caroline,
Prodhomme Mélanie K.,
Burlet Delphine,
Kashiwagi Ayaka,
Petrilli Virginie,
Puisieux Alain,
Seimiya Hiroyuki,
Tissier Agnès
Publication year - 2022
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.15389
Subject(s) - dna repair , dna damage , dna damage repair , epithelial–mesenchymal transition , biology , tumor microenvironment , cancer research , cancer , transcription factor , cancer stem cell , tumor initiation , cancer cell , dna , microbiology and biotechnology , bioinformatics , stem cell , tumor cells , genetics , gene , metastasis
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.