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Cell Growth & Differentiation Vol. 10, 155-162, March 1999
© 1999 American Association for Cancer Research

Dose-dependent Effects of DNA-damaging Agents on p53-mediated Cell Cycle Arrest1

Daniel Chang, Feng Chen, Fenfen Zhang, Bruce C. McKay and Mats Ljungman2

Department of Radiation Oncology, Division of Cancer Biology, University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan 48109-0582

We examined the dose-dependent effects of DNA-damaging agents on G1 arrest in isogenic human cell lines differing in their p53 status. As expected, 5 or 20 Gy of ionizing radiation induced a p53-dependent G1 arrest. In contrast, UV light or actinomycin D induced a modest G1 arrest that was p53-dependent only at lower doses. At higher doses, cells were arrested in G1 in a p53-independent manner coinciding with inhibition of RNA synthesis and abolished cyclin E expression. Interestingly, expression of cyclin E was enhanced after exposure to moderate doses of UV light and actinomycin D, and this enhancement was suppressed by wild-type p53. We propose that agents inducing transcription-blocking DNA lesions will at higher doses inhibit the progression of cells into S phase by a p53-independent mechanism involving the attenuation of E2F-mediated transcription of genes, such as cyclin E.




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Molecular Cancer Research Cell Growth & Differentiation
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