Abstract:Objective：To investigate the methylation status of antioncogene protocadherin10 promoter in hepatoma cell line HepG2 and the relationship with the regulation of HBV X protein (HBx). Methods：The expressions of PCDH10 gene in HepG2 cells before and after the treatment with demethylating agent 5-aza-2′-deoxycytidine combined histone deacetylase inhibitors trichostatin A were detected by using reverse transcription PCR (RT-PCR). The methylation levels of PCDH10 promoter CGI (CpG island) were detected by methylation-specific PCR (MSP). The methylated CG sites were specifically detected by bisulphite sequencing PCR (BSP). The transcriptional levels and the methylation status of PCDH10 in HepG2 cells treated by recombinant adenoviruses expressing HBx protein were also detected by MSP. Results：PCDH10 gene was silenced in HepG2 cells and aberrant hypermethylation of PCDH10 promoter CGI was detectable in HepG2 cells. The transcriptional silence of PCDH10 could be partly reversed by Aza with pharmacologic demethylation and the expression of PCDH10 mRNA was up-regulated. No influences on hypermethylation of PCDH10 in HepG2 cells by the expression of HBx protein was found. Conclusion：Aberrant hypermethylation of PCDH10 promoter CGI may result in transcriptional silence in HepG2 cells. However, no correlation was found between the expression of HBx protein and aberrant methylation of PCDH10.