Emodin induces apoptosis of human cervical cancer hela cells via intrinsic mitochondrial and extrinsic death receptor pathway

• Published in: Cancer cell international Vol. 13; no. 1; p. 71
• Main Authors: Yaoxian, Wang, Hui, Yu, Yunyan, Zhang, Yanqin, Liu, Xin, Ge, Xiaoke, Wu
• Format: Journal Article
• Language: English
• Published: England BioMed Central 16.07.2013; BioMed Central Ltd
• Subjects: Apoptosis; Cell growth; Cervical cancer; Enzymes; Primary Research; Proteins
• ISSN: 1475-2867; 1475-2867
• DOI: 10.1186/1475-2867-13-71

Emodin is a natural anthraquinone derivative isolated from the Rheum palmatum L. 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 mechanisms involved. Relative cell viability was assessed by MTT assay after treatment with emodin. Cell apoptosis was detected with TUNEL, Hoechst 33342 staining and quantified with flow cytometry using annexin FITC-PI staining. The percentage of apoptotic cells was 0.8, 8.2, 22.1, and 43.7%, respectively. The mRNA levels of Caspase-9, -8 and -3 detected by Real-time PCR after treatment with emodin were significantly increased. 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-8 and Pro-caspase-3. We conclude that the emodin inhibited HeLa proliferation by inducing apoptosis through the intrinsic mitochondrial and extrinsic death receptor pathways.