How ever, the results regarding correlations of MUC2 expres sion in cancer are contradictory. Given that the aberrant expression of MUC2, it is conceivable that MUC2 may be also involved in the de velopment of cellular differentiation in Hepatocellular Carcinoma. Relatively little selleck chemicals is known, however, about the mechanisms responsible for regulation of MUC2 expression in HCC. MUC2 gene regulation mechanism disclosed that DNA methylation and his tone modification in the 5 flanking region of the MUC2 promoter may play an important role. MUC2 are highly submitted to DNA methylation and histone modifications, and MUC2 repression by cell specified methylation is controlled by DNA methyltransferase 1 and dramatically impairs their activation by the Inhibitors,Modulators,Libraries transcription factor Sp1 in epithelial cancer cells.
MUC2 expression Inhibitors,Modulators,Libraries in gastric cells is regulated by promoter methylation with Inhibitors,Modulators,Libraries two specific CpG sites. And the low methylation status of MUC2 gene plays a predominant role in high level MUC2 expression in mu cinous colorectal cancer. The histone H3 modifica tion could play an important role in MUC2 gene expression, possibly affecting DNA methylation in pan creatic neoplasm. It implied that the promoter methylation of MUC2 could play a particularly important regulatory role for MUC2 expression in carcinogenesis. So far the few studies conducted focused on MUC2 methylation and no data are available regarding MUC2 in HCC. In this study, we examined the expression of MUC2 with respect to the promoter methylation in HCC.
Materials and methods Patients and tissue Inhibitors,Modulators,Libraries samples All of these cases were surgically resected from 74 patients with HCC, and were obtained from our departments and affiliated hospitals. The tissues samples were flash frozen in liquid nitrogen immediately after surgical resection. The matched Inhibitors,Modulators,Libraries non HCC tissues were obtained from the liver 3 cm away from tumors and were confirmed to be tumor free by microscopic exam ination. The patients consisted of 65 men and 9 women, ranging in age from 27 to 70 years. All tumors were histologically diagnosed as HCC according to the Edmondson Steiner classification system. Written informed consent was obtained from each patient, sellectchem and the protocol of the study was approved by the local ethics committee of Soochow University. Cell culture and treatment The HCC cancer cell lines were kept in our laboratory. The cells were cultured in RPMI medium plus 10% fetal bovine serum in a humidi fied 37 C incubator containing 5% CO2. They were plated and treated with final concentration of 10 uM 5 Aza 2 deoxycytidine and 400 ng/ml Trichostatin A. The fresh medium was changed every 24 hours to maintain the 5 Aza CdR and TSA concentration. RNA was isolated 3 days after treatment. DMSO was being a blank control.