Contributors: Département cancer environnement (Centre Léon Bérard - Lyon); Centre Léon Bérard Lyon; Développement Cancer et Thérapies Ciblées Lyon (LabEx DEVweCAN); Université de Lyon; Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL); Centre Léon Bérard Lyon -Université Claude Bernard Lyon 1 (UCBL); Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS); Université de Versailles Saint-Quentin-en-Yvelines (UVSQ); Japan Agency for Medical Research and Development, AMED: 21cm0106184h0001; Japan Society for the Promotion of Science, KAKEN: 20H04789, 20K21555; Ligue Contre le Cancer: ANR‐10‐LABX‐0061, ANR‐17‐CONV‐0002, EL2016.LNCC/AIP, EL2019.LNCC/AIP; Nippon Foundation; This work was supported by the Ligue contre le Cancer (EL2016.LNCC/AIP and EL2019.LNCC/AIP), ANR‐17‐CONV‐0002, and ANR‐10‐LABX‐0061. This work was also supported by JSPS KAKENHI (20K21555 and 20H04789), AMED P‐CREATE (21cm0106184h0001) and funding from Nippon Foundation to HS; ANR-17-CONV-0002,PLASCAN,Institut François Rabelais pour la recherche multidisciplinaire sur le cancer(2017)
نبذة مختصرة : International audience ; 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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