OBJECTIVE: To gain insights into the role of forkhead box protein 3 (Foxp3) in the pathogenesis of hepatocellular carcinoma (HCC) by performing a comparative analysis of Foxp3 mRNA expression and promoter methylation status in HCC and normal liver tissues. METHODS: Thirty-nine HCC and 13 normal liver tissue specimens were evaluated by real-time quantitative PCR and pyrosequencing to measure the expression of Foxp3 mRNA and determine the methylation status of its promoter, respectively. Statistical analyses of the data were conducted by rank-sum test and Spearman's rank correlation coefficient test. RESULTS: The HCC specimens showed significantly higher mRNA expression of Foxp3 (vs. normal liver tissues, Z =-2.770, P =0.0056). Moreover, the HCC specimens showed significant hypomethylation of the Foxp3 promoter site A (vs. normal liver tissues, Z =2.118, P =0.0339), and the Foxp3 mRNA level was negatively correlated with the methylation of site A (rs =-0.344, P =0.046). None of the other four sites in the Foxp3 promoter showed a significant difference in methylation, and the overall methylation was not significantly different between the HCC and normal liver tissues. CONCLUSION: Overexpression and low methylation of Foxp3 may be involved in the oncogenic and progression processes of HCC.
OBJECTIVE: To gain insights into the role of forkhead box protein 3 (Foxp3) in the pathogenesis of hepatocellular carcinoma (HCC) by performing a comparative analysis of Foxp3 mRNA expression and promoter methylation status in HCC and normal liver tissues. METHODS: Thirty-nine HCC and 13 normal liver tissue specimens were evaluated by real-time quantitative PCR and pyrosequencing to measure the expression of Foxp3 mRNA and determine the methylation status of its promoter, respectively. Statistical analyses of the data were conducted by rank-sum test and Spearman's rank correlation coefficient test. RESULTS: The HCC specimens showed significantly higher mRNA expression of Foxp3 (vs. normal liver tissues, Z =-2.770, P =0.0056). Moreover, the HCC specimens showed significant hypomethylation of the Foxp3 promoter site A (vs. normal liver tissues, Z =2.118, P =0.0339), and the Foxp3 mRNA level was negatively correlated with the methylation of site A (rs =-0.344, P =0.046). None of the other four sites in the Foxp3 promoter showed a significant difference in methylation, and the overall methylation was not significantly different between the HCC and normal liver tissues. CONCLUSION: Overexpression and low methylation of Foxp3 may be involved in the oncogenic and progression processes of HCC.