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

Abstract

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 μM) 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.