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
- Ligue contre le Cancer [EL2016]
- LNCC/AIP [ANR--17--CONV--0002, ANR--10--LABX--0061]
- JSPS KAKENHI [20K21555, 20H04789, AMED P--CREATE (21cm0106184h0001)]
- Nippon Foundation
- Agence Nationale de la Recherche (ANR) [ANR-17-CONV-0002] Funding Source: Agence Nationale de la Recherche (ANR)
- Grants-in-Aid for Scientific Research [20H04789, 20K21555] Funding Source: KAKEN
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据