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KMID : 0624620140470040221
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BMB Reports
2014 Volume.47 No. 4 p.221 ~ p.226
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Nutlin-3 downregulates p53 phosphorylation on serine392 and induces apoptosis in hepatocellular carcinoma cells
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Shi Xinli
Liu Jingli
Ren Laifeng
Mao Nan
Tan Fang
Ding Nana
Yang Jing
Li Mingyuan
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Abstract
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Drug-resistance and imbalance of apoptotic regulation limit chemotherapy clinical application for the human hepatocellular carcinoma (HCC) treatment. The reactivation of p53 is an attractive therapeutic strategy in cancer with disrupted-p53 function. Nutlin-3, a MDM2 antagonist, has antitumor activity in various cancers. The post-translational modifications of p53 are a hot topic, but there are some controversy ideas about the function of phospho-Ser392-p53 protein in cancer cell lines in response to Nutlin-3. Therefore, we investigated the relationship between Nutlin-3 and phospho-Ser392-p53 protein expression levels in SMMC-7721 (wild-type TP53) and HuH-7 cells (mutant TP53). We demonstrated that Nutlin-3 induced apoptosis through down-regulation phospho-Ser392-p53 in two HCC cells. The result suggests that inhibition of p53 phosphorylation on Ser392 presents an alternative for HCC chemotherapy.
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KEYWORD
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Apoptosis, Human hepatocellular carcinoma, Nutlin-3, p53, Phospho-Ser392-p53
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