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miR-29c 靶向 TNFAIP3,抑制乙型肝炎病毒相关肝细胞癌的细胞增殖并诱导细胞凋亡。

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

机构信息

Department of Microbiology, Shandong University School of Medicine, Jinan 250012, PR China.

出版信息

Biochem Biophys Res Commun. 2011 Aug 5;411(3):586-92. doi: 10.1016/j.bbrc.2011.06.191. Epub 2011 Jul 6.

Abstract

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.

摘要

最近的研究表明,微小 RNA-29c(miR-29c)参与多种生物学过程,包括致癌作用。在这里,我们报告 miR-29c 在乙型肝炎病毒(HBV)相关肝细胞癌(HCC)细胞系以及与相应对照相比的临床组织中显著下调。肿瘤坏死因子α诱导蛋白 3(TNFAIP3)是炎症和免疫的关键调节因子,与 miR-29c 水平呈负相关,并被鉴定为 miR-29c 的靶标。在 HepG2.2.15 细胞中转染 miR-29c 可有效抑制 TNFAIP3 表达和 HBV DNA 复制,抑制细胞增殖并诱导细胞凋亡。我们得出结论,miR-29c 可能通过靶向 TNFAIP3 作为肿瘤抑制性 microRNA 在 HBV 相关 HCC 的发生和发展中发挥重要作用。因此,miR-29c 和 TNFAIP3 代表了用于预防和治疗 HBV 感染的关键诊断标志物和潜在治疗靶点。

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