Investigation On Apoptosis Of Human Cervical Cancer Hela Cells Through Cativating Casepase Induced By Emodin

Aims The aim of the present study was to investigate the effect of emodin on the apoptosis of the human cervical cancer line HeLa and to identify the mechanism involved.Methods and Result Relative cell viability assessed by MTT assay after treatment with emodin (0,10,20,30,40and50μM) for24,48, and72h was100,97,85,74,61,52%for24h,100,94,75,59,46,31%for48h, and100,87,66,44,32,16%for72h, respectively. Cell apoptosis was detected with TUNEL, Hoechst33342staining and quantified with flow cytometry using annexin FITC-PI staining at48h after treatment with emodin (0,20,40and80μM). The percentage of apoptotic cells was0.8,8.2,22.1, and43.7%, respectively. The mRNA levels of Caspase-9,-8and-3detected by Real-time PCR after treatment with emodin (0,20,40and80μM) for48h were significantly increased. The levels of apoptosis-related proteins including Cytochome c, apoptotic protease activating factor1(Apaf-1), Caspase-9, Fas, FasL, FADD, Caspase-8, and Caspase-3were evaluated in emodin-treated cells. Emodin increased the protein levels of Cytochome c, Apaf-1, Fas, FasL, and FADD but decreased the protein levels of Pro-caspase-9, Pro-caspase-8and Pro-caspase-3.Conclusions We conclude that emodin inhibits HeLa proliferation by inducing apoptosis and this antitumor effect of emodin is possibly mediated by the intrinsic mitochondrial and the extrinsic death receptor pathways.