Emodin elicits cytotoxicity in human lung adenocarcinoma A549 cells through inducing apoptosis.

This study investigated the mechanism of the cytotoxic effect of emodin, an active anthraquinone, on human lung adenocarcinoma A549 cells. In vitro growth inhibition and suppression on colony forming were used to evaluate the effects of emodin on A549 cells. Emodin's ability in changing the expressions of apoptosis-related genes was studied by real-time RT-PCR. Emodin could significantly inhibit the growth of A549 cells with IC50 = 16.85 μg/ml (~60 μM). It also concentration dependently inhibited the colony-forming ability of A549 cells with IC50 = 7.60 μg/ml (~30 μM). Hallmarks of apoptosis, such as single-strand DNA breakage and DNA fragmentation, were observed in A549 cells treated with emodin. Emodin (72 h) treatment could up-regulate the gene expression of FASL (p < 0.05) and down-regulate the gene expression of C-MYC (p < 0.01), but induce no significant changes in the gene expressions of MCL1, GAPDH, BAX and CCND1. These results suggest that emodin could induce growth inhibition and apoptosis in A549 cells through modifying the extrinsic apoptotic pathways and the induction of cell cycle arrest.