Journal Article

Decrease in the frequency of X-ray-induced mutation by wild-type p53 protein in human osteosarcoma cells.

N Yamagishi, J Miyakoshi and H Takebe

in Carcinogenesis

Volume 18, issue 4, pages 695-700
Published in print April 1997 | ISSN: 0143-3334
Published online April 1997 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/18.4.695
Decrease in the frequency of X-ray-induced mutation by wild-type p53 protein in human osteosarcoma cells.

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Tumor suppressor p53 protein acts as a checkpoint factor following DNA damage. Inactivation of checkpoint control may increase the frequency of mutation following DNA damage, resulting in tumor progression. Here we examine whether wild-type (wt) p53 protein suppresses X-ray-induced mutations using an isopropyl-beta-D-thiogalactopyranoside (IPTG)-regulated p53 expression system in human osteosarcoma Saos-2 cells. Frequency of X-ray-induced mutations in the hypoxanthine-guanine phosphoribosyl transferase gene was enhanced about 10 and 20 times by 1 and 2 Gy respectively in cells without expression of wt p53 protein, while enhancement of mutations by X-rays was slight in cells with expression of wt p53 protein. Furthermore, arrest at the G/S boundary was induced by X-ray irradiation when p53 protein was expressed by treatment with IPTG. These findings suggest that wt p53 protein has a function in maintaining genomic stability after X-ray irradiation through the G1 checkpoint and loss of p53 function(s) may lead to tumor progression in multi-step tumorigenesis.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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