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Accumulating evidence has identified a mechanism potentially responsible for the inactivation of tumor suppressor genes, namely transcriptional silencing by aberrant methylation of CpG islands.The role of aberrant methylation of GPX3 promoters in the hepatocellular carcinoma (HCC) is not yet clear.Therefore, we investigated the association of the status of GPX3promoter methylation and GPX3 protein expression with the clinicopathological progression of HCC.76.7% (46/60) showed at the promoter region and displayed significantly lower levels of GPX3 mRNA and protein expression.Concordance with GPX3 mRNA, protein expression was observed in 10 of 60 tumors which showed low or undetectable expression.Promoter methylation was detected in 46 of 60 (76.7%) tumors, while no GPX3 gene promoter methylation was observed in the matched noncancerous specimens.There was a negative correlation correlation between promoter methylation and mRNA expression of GPX3 gene (P<0.05).In comparison with clinicopathological data, both the mRNA and protein appeared to be significantly associated with the portal tumor thrombosis, metastasis and differentiation.In additional, the methylation showed a relation with portal tumor thrombosis, metastasis and differentiation.Our results suggest that methylation appears to be mechanism for inactivation of GPX3-possibly leading to subsequent carcinogenesis and progression of HCC.