期刊
ONCOGENE
卷 19, 期 17, 页码 2165-2170出版社
STOCKTON PRESS
DOI: 10.1038/sj.onc.1203573
关键词
p21; mitosis; endoreduplication; spindle checkpoint control; senescence
资金
- NCI NIH HHS [R37CA40333, R01CA62099] Funding Source: Medline
Induction of a cyclin-dependent kinase inhibitor p21(Wafl/) (Cip1/Sdi1) is an integral part of cell growth arrest associated with senescence and damage response, p21 overexpression from an inducible promoter resulted in senescence-like growth arrest in a human fibrosarcoma cell line. After release from p21-induced growth arrest, cells reentered the cell cycle but displayed growth retardation, cell death and decreased clonogenicity. The failure to form colonies was associated with abnormal mitosis and endoreduplication in the recovering cells and was correlated with the induced level of p21 and the duration of p21 induction. p21 induction was found to inhibit the expression of multiple proteins involved in the execution and control of mitosis, p21-induced depletion of the cellular pools of mitosis-control proteins nas followed by asynchronous resynthesis of such proteins after release from p21, which explains the observed mitotic abnormalities. Genetic destabilization in cells recovering from p21-induced growth arrest may conceivably play a role in carcinogenesis and tumor progression.
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