期刊
NUCLEUS
卷 8, 期 3, 页码 268-274出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/19491034.2017.1292191
关键词
confined migration; DNA damage; ESCRT; lamina; nuclear envelope rupture
类别
资金
- National Institutes of Health [R01 HL082792, U54 CA210184]
- Department of Defense Breast Cancer Research Program [BC150580]
- National Science Foundation (CAREER Award) [CBET-1254846]
Cell migration through tight spaces can induce substantial deformations of the nucleus and cause nuclear envelope (NE) rupture, resulting in uncontrolled exchange of nuclear and cytosolic proteins. These events can cause DNA damage and, in severe cases, nuclear fragmentation, challenging the integrity of the genomic material. Cells overcome NE ruptures during interphase by repairing the NE using components of the endosomal sorting complexes required for transport (ESCRT) machinery. Paralleling the molecular mechanism used during NE reformation in late mitosis, ESCRT-III subunits and the associated AAA-ATPase VPS4B are recruited to NE rupture sites and help restore NE integrity. While these findings are common to many cell types, they are particularly relevant in the context of cancer metastasis, where nuclear deformation and rupture could drive genomic instability in invading cells and further promote cancer progression. At the same time, inhibiting NE repair may offer new therapeutic approaches to specifically target invasive cancer cells.
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