Emodin induces apoptosis of prostate cancer cells via cysteinyl aspartate-specific protease-independent pathway

Abstract

Objective To investigate the effects of emodin on apoptosis and the expression of apoptosis inducing factor(AIF)and endonuclease G(Endo G)in prostate cancer cells and the mechanism. Methods The prostate cancer cells cultured in vitro were divided into 4 groups:blank control group, emodin group, cysteinyl aspartate-specific protease(Caspase)inhibitor group and emodin combined with caspase inhibitor group.Methyl thiazol tetrazolium(MTT)colorimetric assay was used to measure the cell viability. The apoptosis of the cells was measured by flow cytometry.The expression of AIF and Endo G mRNA and protents was detected by real-time quantitative polymerase chain reaction(Real-time PCR)and Western blotting, respectively. Results MTT results showed that the cell growth was inhibited by emodin in a dose -dependent and time-dependent manner when the concentration was upper than 20μmol/L(P<0. 05). The inhibiting rate in prostate cancer cells after 48 and 96 hours were(59. 76±3. 90)% and(71. 77± 3. 50)% when the Emodin concentration was 160μmol/L.Emodin significantly increased the apoptosis rate in prostate cancer cells compared with blank control group[(22. 54±2. 32)% vs.(4. 54±1. 26)%,P< 0. 05].Emodin combined with caspase inhibitor can also significantly increase the apoptosis rate in prostate cancer cells compared with blank control group[(15. 65±1. 84)% vs.(4. 54±1. 26)%,P< 0. 05].Compared with blank control group,emodin, with or without caspase inhibitor,significantly upregulated the expressions of AIF and Endo G mRNA and protein(P< 0. 05). Conclusion Emodin could induce apoptosis of prostate cancer cells via caspase-independent AIF/Endo G pathway. Key words: Emodin; Prostate cancer; Apoptosis; Endonuclease G