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Reversal of p53-induced cell-cycle arrest

✍ Scribed by Stewart Bates; Emma S. Hickman; Karen H. Vousden

Publisher: John Wiley and Sons
Year: 1999
Tongue: English
Weight: 210 KB
Volume: 24
Category: Article
ISSN: 0899-1987
DOI: 10.1002/(sici)1098-2744(199901)24:1<7::aid-mc2>3.0.co;2-5

No coin nor oath required. For personal study only.

✦ Synopsis

Activation of the tumor suppressor protein p53 can lead to arrest in both G 1 and G 2 stages of the cell cycle and, in some cells, to apoptotic cell death. In this study, we showed that the p53 response to a chemotherapeutic drug, actinomycin D, was reversible in both normal and tumor cells, even when a substantial proportion of tumor cells were undergoing apoptosis. Despite the clear reversibility of the p53-induced cell-cycle arrest after removal of actinomycin D, a substantial proportion of the cells arrested in G 2 failed to resume normal cell-cycle progression and underwent another round of DNA synthesis. This endoreduplication probably reflects a function of the cyclin-dependent kinase inhibitor p21 Waf1/Cip1 , which is expressed in response to p53. Our observation that this abnormal re-replication of DNA occurred in both transformed and untransformed cells after reversal of a p53 response may have implications for the eventual outcome of tumor therapies in which p53 is transiently expressed in a substantial number of normal as well as tumor cells.

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