Abstract：
BACKGROUND:Previous studies suggest that human RAD9 (hRad9), encoding a DNA damage checkpoint molecule, which is frequently amplified in epithelial tumor cells of breast, lung, head and neck cancer, participates in regulation of the tumor suppressor p53-dependent transactivation of pro-survival P21WAF1. This study examined the exact mechanism of the hRad9 function, especially through the phosphorylation of the C-terminus, in the transcription regulation of P21WAF1. RESULTS:The transfection of phosphorylation-defective hRAD9 mutants of C-terminus resulted in reduction of the p53-dependent P21WAF1 transactivation; the knockdown of total hRad9 elicited an increased P21WAF1 mRNA expression. Immunoprecipitation and a ChIP assay showed that hRad9 and p53 formed a complex and both were associated with two p53-consensus DNA-binding sequences in the 5' region of P21WAF1 gene. The association was reduced in the experiment of phosphorylation-defective hRAD9 mutants. CONCLUSION:The present study indicates the direct involvement of hRad9 in the p53-dependent P21WAF1 transcriptional mechanism, presumably via the phosphorylation sites, and alterations of the hRad9 pathway might therefore contribute to the perturbation of checkpoint activation in cancer cells.
journal_name
BMC Mol Bioljournal_title
BMC molecular biologyauthors
Ishikawa K,Ishii H,Murakumo Y,Mimori K,Kobayashi M,Yamamoto K,Mori M,Nishino H,Furukawa Y,Ichimura Kdoi
10.1186/1471-2199-8-37subject
Has Abstractpub_date
2007-05-21 00:00:00pages
37issn
1471-2199pii
1471-2199-8-37journal_volume
8pub_type
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