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miR-376a 抑制肝癌细胞增殖并诱导其凋亡。

miR-376a suppresses proliferation and induces apoptosis in hepatocellular carcinoma.

机构信息

Department of Biochemistry and Molecular Biology, Second Military Medical University, Shanghai, China.

出版信息

FEBS Lett. 2012 Jul 30;586(16):2396-403. doi: 10.1016/j.febslet.2012.05.054. Epub 2012 Jun 7.

DOI:10.1016/j.febslet.2012.05.054
PMID:22684007
Abstract

MicroRNAs are known to be involved in the pathogenesis of hepatocellular carcinoma (HCC). This study aims to explore the potential biological function of miR-376a, which was found to be inhibited after partial hepatectomy, in HCC. We discovered that miR-376a was frequently down-regulated in HCC cell lines and HCC tissues, while higher relative level of miR-376a was significantly associated with high serum AFP level. Over-expression of miR-376a not only inhibited proliferation but induced apoptosis in Huh7 cells. Additionally, p85α (PIK3R1) was identified as a direct and functional target of miR-376a in Huh7 cells. Moreover, we confirmed that p85α and miR-376a were inversely correlated in HCC. These findings suggest that down-regulation of miR-376a may contribute to the development of HCC by targeting p85α.

摘要

微小 RNA 被认为参与了肝细胞癌 (HCC) 的发病机制。本研究旨在探讨 miR-376a 的潜在生物学功能,该 miR-376a 在部分肝切除后被发现受到抑制,在 HCC 中。我们发现 miR-376a 在 HCC 细胞系和 HCC 组织中经常下调,而相对较高水平的 miR-376a 与高血清 AFP 水平显著相关。miR-376a 的过表达不仅抑制了 Huh7 细胞的增殖,还诱导了其凋亡。此外,p85α (PIK3R1) 被鉴定为 Huh7 细胞中 miR-376a 的直接和功能靶标。此外,我们证实 p85α 和 miR-376a 在 HCC 中呈负相关。这些发现表明,miR-376a 的下调可能通过靶向 p85α 促进 HCC 的发展。

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