Studies on the epigenetic mechanism of arsenic carcinogenesis on human liver cancer cell line

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In this study, we investigated the mechanism involved in arsenic-induced carcinogenesis focusing on epigenetic regulations of the tumor suppressor gene p16^<1NK4a> in human urothelial cell lines. The results showed that arsenic exposure induced a significant decrease in expression of p16^<1NK4a> associated with an increase in the level of trimethylated histone H3 lysine 27 (H3K27), a transcription-suppressive histone modification, in the promoter region. The results also showed that arsenic exposure induced a significant increase in expression of H3K27 histone methyltransferase EZH2. These results suggested that the decreased expression of p16^<1NK4a> through histone modification is associated with arsenic-induced carcinogenesis in human urothelial cell lines.