A study on the response of oral mucosa to reactive oxygen species and its application to the prevention against oral cancer.

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In order to investigate the mechanism how reactive oxygen species (ROS) induce carcinogenesis of keratinocytes, normal human kerainocytes (NHEK) and oral squamous carcinoma cells (SCCs) were treated with hydrogen peroxide, and compared for the expressions of cellular senescence-associated molecules that is thought to be one of the tumor suppressor mechanisms. Hydrogen peroxide increased the expressions of senescence associated-beta-galactosidase and p16(INK4a) and induced the growth arrest in G0/G1 phase, in NHEK, but not SCC cells. Methylation level in p16 (INK4a) promoter was reduced with hydrogen peroxide in NHEK, but not SCCs. Methylation inhibitor 5-Azac enhanced the expression of p16 (INK4a) in NHEK, but not SCCs. The expression of DNA methyltransferase DNMT1 was suppressed in NHEK, but not SCCs. The inhibition of cellular senescence through the epigenetic modification on p16 (INK4a) expression may play an important role in carcinogenesis of keratinocytes.