Abstract
4-O-methyl-ascochlorin (MAC) is a methylated derivative of the prenyl-phenol antibiotic ascochlorin, which was isolated from the incomplete fungus Ascochyta viciae. We have recently shown that MAC promotes apoptotic cell death by inhibiting c-Myc expression in K562 leukemia cells, but the effects of MAC on autophagy are still unknown. Treatment of MAC significantly increased LC3 expression and autophagic vesicle formation by western blot and acridine orange staining. Also, we examined the possible mechanisms underlying MAC induced autophagy. We found that MAC suppressed c-Myc expression by inhibiting CIP2A (regulator of c-Myc) protein synthesis. This result suggests that the downregulation of c-Myc expression plays the role of inducing apoptosis and autophagy by MAC treatment in human leukemia cells. These findings significantly contributed to the understanding of the mechanism that accounts for the anticancer activity of MAC, and it may be novel anti-cancer therapeutic agents for leukemia cells.
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