Carcinogenesis, Teratogenesis & Mutagenesis ›› 2009, Vol. 21 ›› Issue (5): 339-343.doi: 10.3969/j.issn.1004-616x.2009.05.003

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Effects of RNAi Targeted to STAT3 on Apoptosis Induction and on STAT3 Signaling in Human Hepatocellular Carcinoma Cells

XU Jia1; ZHANG Yin-juan2;LU Gang3;SHAN Bao-en3;   

  1. 1. School of Medicine in Biochemistry, Ji'nan University Guangzhou,510632;2. Clinical Laboratory,People's Hospital of Linfen City, Linfen 041000,Shanxi;3. Research Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, China
  • Received:2009-03-20 Revised:2009-05-17 Online:2009-09-30 Published:2009-09-30
  • Contact: SHAN Bao-en

Abstract: BACKGROUND AND AIM: To investigate the effects of RNAi targeted to STAT3 on apoptosis induction and on STAT3 signaling in human hepatocellular carcinoma cell line SMMC7721. The research provided theoretical and experimental basis for further development and clinical application of targeting STAT3 signaling pathway therapy for cancer. MATERIALS AND METHODS: Applying RNAi technique to specifically silence STAT3 gene in SMMC7721 cells, and expression of STAT3 protein in cells was determined by Western blot. Effect of RNAi on SMMC7721 apoptosis was determined by flow cytometry. Expressions of apoptosis-associated genes survivin and bcl-2 were determined by semi-quantitative RT-PCR. RESULTS: RNAi technology could effectively and specifically silence the expression of STAT3. Compared to the control group, the apoptosis rate was significantly increased after RNAi silencing STAT3 (P<0.01). Expressions of survivin and bcl-2 mRNA were significantly inhibited compared to the control group (P<0.01). CONCLUSION: RNAi technology targeted to STAT3 could effectively silence STAT3 expression in SMMC7721. RNAi targeted to STAT3 induced apoptosis by down-regulating the expressions of bcl-2 and survivin mRNA.

Key words: RNAi, STAT3, hepatocellular carcinoma, signal transduction, apoptosis

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