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Carcinogenesis, Vol. 22, No. 4, 573-578, April 2001
© 2001 Oxford University Press

CANCER BIOLOGY

p53 is dispensable for UV-induced cell cycle arrest at late G1 in mammalian cells

Mai A. Al-Mohanna, Fahad M. Al-Khodairy, Zbigniew Krezolek, Per-Anders Bertilsson, Khalid A. Al-Houssein and Abdelilah Aboussekhra,1

King Faisal Specialist Hospital and Research Center, Biological and Medical Research Department, MBC No. 03, PO Box 3354, Riyadh 11211, Saudi Arabia

Genotoxic agents, including {gamma}-rays and UV light, induce transient arrest at different phases of the cell cycle. These arrests are required for efficient repair of DNA lesions, and employ several factors, including the product of the tumor suppressor gene p53 that plays a central role in the cellular response to DNA damage. p53 protein has a major function in the {gamma}-ray-induced cell cycle delay in G1 phase. However, it remains uncertain as to whether p53 is also involved in the UV-mediated G1 delay. This report provides evidence that p53 is not involved in UV-induced cellular growth arrest in late G1 phase. This has been demonstrated in HeLa cells synchronized at the G1/S border by aphidicolin, followed by UV exposure. Interestingly, the length of this p53-independent G1 arrest has been shown to be UV dose-dependent. Similar results were also obtained with other p53-deficient cell lines, including human promyelocytic leukemia HL-60 and mouse p53 knock-out cells. As expected, all of these cell lines were defective in {gamma}-ray-induced cell growth arrest at late G1. Moreover, it is shown that in addition to cell cycle arrest, HL-60 cells undergo apoptosis in G1 phase in response to UV light but not to {gamma}-rays. Together, these findings indicate that p53- compromised cells have a differential response following exposure to ionizing radiation or UV light.


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