miR-29c targets TNFAIP3, inhibits cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma

• DOI: 10.1016/j.bbrc.2011.06.191
• Publication Date: 2011-07-07T18:41:18Z
• Authors: Chun-Mei Wang; Yan Wang; Chun-Guang Fan; Fei-Fei Xu; Wen-Sheng Sun; Yu-Gang Liu; Ji-Hui Jia
• Keywords: Hepatitis B virus; 0303 health sciences; Carcinoma, Hepatocellular; Hepatitis B Surface Antigens; Liver Neoplasms; Intracellular Signaling Peptides and Proteins; Down-Regulation; Nuclear Proteins; Apoptosis; Transfection; 3. Good health; DNA-Binding Proteins; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Cell Transformation, Neoplastic; Cell Line, Tumor; Biomarkers, Tumor; Humans; Hepatitis B e Antigens; Tumor Necrosis Factor alpha-Induced Protein 3; Cell Proliferation

Recent studies have revealed that microRNA-29c (miR-29c) is involved in a variety of biological processes including carcinogenesis. Here, we report that miR-29c was significantly downregulated in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) cell lines as well as in clinical tissues compared with their corresponding controls. Tumor necrosis factor alpha-induced protein 3 (TNFAIP3), a key regulator in inflammation and immunity, was found to be inversely correlated with miR-29c levels and was identified as a target of miR-29c. Overexpression of miR-29c in HepG2.2.15 cells effectively suppressed TNFAIP3 expression and HBV DNA replication as well as inhibited cell proliferation and induced apoptosis. We conclude that miR-29c may play an important role as a tumor suppressive microRNA in the development and progression of HBV-related HCC by targeting TNFAIP3. Thus miR-29c and TNFAIP3 represent key diagnostic markers and potential therapeutic targets for the prevention and treatment of HBV infection.