Effect and Mechanism of Emodin on Apoptosis and Cycle of HCT116 Cells

OBJECTIVE To investigate the effect of emodin on human colon cancer cell line HCT116 and its molecular mechanism. METHODS The inhibitory effects of emodin on the viability of HCT116 cells were measured by CCK8 assay. Apoptosis rates of HCT116 cells were determined by flow cytometry. The cell cycle and the level of reactive oxygen species (ROS) in the fluorescent probe DCF-DA were detected by flow cytometry. The protein levels of Bax，Bcl-2，p-ERK1/2，ERK1/2 and c-Myc were determined by Western blot. RESULTS Treatment with emodin of 0， 25， 50， 100， 200， 300 μmol/L for 24 h significantly reduced the viability of HCT116 cells. Emodin promoted the apoptosis of HCT116 cells， blocked cell growth cycle in G0/G1 phase and induced the production of ROS， significantly. Western blot results showed that emodin promoted the up-regulation of Bax/Bcl-2 expression and inhibited the expression of c-Myc and p-ERK/ERK. CONCLUSION Emodin inhibits the proliferation of HCT116 cells， promotes cell apoptosis， induces cell cycle arrest in G1/G0 phase and ROS production， by promoting Bax/Bcl-2 expression and inhibiting c-Myc， p-ERK/ERK expression.