| Objective:To investigate TSLC1and MAL gene mRNA expression and promoter methylation status in breast cancer tissue, and to analysis the association between TSLC1and MAL gene in the occurrence and development of breast cancer.Methods:Real-time fluorescence quantitative polymerase chain reaction and methylation-specific PCR were used to detect mRNA expression and promoter methylation of the TSLC1and MAL gene in42cases breast carcinoma samples,42cases matched tumor-adjacent tissue samples and10cases benign diseased tissue, respectively. Then we studied the association between TSLC1and MAL gene expression and their DNA methylation, respectively and the correlation between changes of the two.Results:The expression of TSLC1and MAL mRNA in breast cancer tissue is0.44and0.66times as much as that in matched tumor-adjacent tissue samples. The methylation rate of the TSLC1and MAL gene is54.8%,9.5%and66.7%,11.9%in breast carcinoma samples and matched tumor-adjacent tissue samples, respectively. The methylation rate is all zero in benign diseased tissue. Methylation of the TSLC1and MAL promoter region in breast carcinoma samples increased significantly compared with matched tumor-adjacent tissue samples and benign diseased tissue (χ2=17.684,9.819; χ2=24.157,11.886; P<0.01). The expression of TSLC1and MAL mRNA in methylated carcinoma samples is0.60and0.71times as much as that in unmethylated carcinoma samples. TSLC1and MAL promoter methylation was observed in51.4%,100%and61.1%,100%in TSLC1mRNA expressed and unexpressed carcinoma samples, respectively, with a significant difference between the two groups (P=0.030, P=0.049<0.05). There is no correlation between TSLC1and MAL gene (χ2=1.145, χ2=1.201; P=0.285, P=0.273<0.05).Conclusion:TSLC1and MAL gene abnormal methylation is one of the reasons for leading to their mRNA expression lossing or down-regulation in breast cancer tissue, playing a relevant role in the development of breast cancer, which may be some of the genes for early diagnosis of breast cancer and therapeutic targets. |