Exogenous S-Adenosyl-L-Methionine Could Inhibit C-Myc Overexpression Induced By As2o3 In Normal Human Liver Hl-7702 Cells

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 c-myc. 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 (0-20 mu M) for 24 hr. However, this elevated c-myc expression is significantly inhibited by 0.2 mu M SAM. Co-treatment of HL-7702 cells with 1.0 mu M As2O3 and 0.2 mu M 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.