| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1930416 | Biochemical and Biophysical Research Communications | 2011 | 7 Pages |
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.
► miR-29c was significantly downregulated in HBV-related HCC. ► TNFAIP3 was found to be inversely correlated with miR-29c levels and identified as a target of miR-29c. ► Overexpression of miR-29c suppressed TNFAIP3. ► miR-29c inhibited HBV DNA replication, cell proliferation and induced apoptosis.
