期刊
CELL CYCLE
卷 8, 期 12, 页码 1888-1895出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.8.12.8606
关键词
cellular senescence; cell cycle arrest; aging; rapamycin; mTOR; TOR
类别
资金
- NIH [1 R41 EY018520-01]
- Russian Foundation for Basic Research (RFBR) [07-04-01537]
- CRDF-RFBR [RUB1-2868-ST-07/07-04-91154]
- Russian Academy of Sciences (MCB RAS).
When the cell cycle is arrested but cellular growth is not, then cells senesce, permanently losing proliferative potential. Here we demonstrated that the duration of cell cycle arrest determines a progressive loss of proliferative capacity. In human and rodent cell lines, rapamycin (an inhibitor of mTOR) dramatically decelerated loss of proliferative potential caused by ectopic p21, p16 and sodium butyrate-induced p21. Thus, when the cell cycle was arrested by these factors in the presence of rapamycin, cells retained the capacity to resume proliferation, once p21, p16 or sodium butyrate were removed. While rapamycin prevented the permanent loss of proliferative potential in arrested cells, it did not force the arrested cells into proliferation. During cell cycle arrest, rapamycin transformed the irreversible arrest into a reversible condition. Our data demonstrate that senescence can be pharmacologically suppressed.
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