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Heat shock induces transient p53-dependent cell cycle arrest at G1/S

Abstract

Heat shock (43°C, 45 min) induced transient nuclear accumulation of p53 in primary human fibroblasts without any clonogenically toxic effects. The accumulation of p53 reached a maximal level 35 h after heat shock, and returned to the basal level within 12 h. Following the increase in p53 level, cell cycle arrest at G1/S was observed in normal fibroblasts, whereas neither nuclear accumulation of p53 nor cell cycle arrest were observed in HeLa cells. By comparing cell cycle patterns of heat-treated mouse cells with different genotypes at the p53 locus (+/+, +/−, −/−), the observed cell cycle arrest at G1/S was demonstrated to be p53-dependent. Cell cycle arrest in normal human fibroblasts continued for nearly 24 h, resulting in a one day delay of cell growth compared with non-treated cells. Following enhancement of the p53 level, the amount of p21/WAF1/CIP1 increased, and the high level of p21 was sustained for almost one day in a cell cycle-independent manner, suggesting the involvement of p21 in the inhibition of cell cycle progression by heat shock.

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Nitta, M., Okamura, H., Aizawa, S. et al. Heat shock induces transient p53-dependent cell cycle arrest at G1/S. Oncogene 15, 561–568 (1997). https://doi.org/10.1038/sj.onc.1201210

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  • DOI: https://doi.org/10.1038/sj.onc.1201210

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