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Arsenic trioxide (As2o3) is known to promote liver and other cancers due to its ability to decrease the level of S-adenosyl-L-methionine (SAM), thus leading to the abnormal expression of oncogene cmyc. The present study investigated the effect of exogenous SAM on As2o3-induced c-myc expression in the normal human liver cells, HL-7702. c-myc expression increased approximately 50% after As2o3 treatments (0-20μM) for 24 hr. However, this elevated c-myc expression is significantly inhibited by 0.2 μM SAM. Co-treatment of HL-7702 cells with 1.0 μM As2o3 and 0.2 μM SAM for 24 and 30 hr, caused prominent inhibitory effects on c-myc overexpression. The results indicate SAM could inhibit c-myc overexpression induced by As2o3 in HL-7702 cells. These findings may be of significance to the exploration of SAM in preventing arsenic carcinogenesis. © 2011 The Pharmaceutical Society of Japan.

Exogenous S-adenosyl-L-methionine Could Inhibit c-myc Overexpression Induced by As2O3 in Normal Human Liver HL-7702 Cells