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miR-542-3p 通过靶向生存素诱导细胞生长停滞。

Induction of growth arrest by miR-542-3p that targets survivin.

机构信息

Graduate School of Biotechnology, Kyung Hee University, Yongin, Republic of Korea.

出版信息

FEBS Lett. 2010 Sep 24;584(18):4048-52. doi: 10.1016/j.febslet.2010.08.025. Epub 2010 Aug 20.

DOI:10.1016/j.febslet.2010.08.025
PMID:20728447
Abstract

Survivin is a protein which functions as a mitotic regulator as well as apoptosis inhibitor. In this study, we show that introduction of synthetic miR-542-3p mimetic reduced both mRNA and protein levels of survivin. In A549 cells, luciferase reporter assay revealed that miR-542-3p targeted predicted binding sites in the 3'-untranslated region (3'-UTR) of survivin. We also demonstrate that ectopic expression of miR-542-3p inhibited cell proliferation by inducing Gap 1 (G1) and Gap 2/Mitosis (G2/M) cell cycle arrest. Collectively, these results suggest that survivin is a direct target of miR-542-3p and growth inhibition by miR-542-3p may have a potential utility as an anti-cancer therapy.

摘要

生存素是一种作为有丝分裂调节剂和细胞凋亡抑制剂发挥功能的蛋白质。在这项研究中,我们表明,合成 miR-542-3p 模拟物的引入降低了生存素的 mRNA 和蛋白水平。在 A549 细胞中,荧光素酶报告基因检测显示 miR-542-3p 靶向生存素 3'非翻译区(3'UTR)中的预测结合位点。我们还证明,miR-542-3p 的异位表达通过诱导 G1(G1)和 G2/有丝分裂(G2/M)细胞周期阻滞来抑制细胞增殖。总之,这些结果表明,生存素是 miR-542-3p 的直接靶标,miR-542-3p 的生长抑制可能具有作为抗癌治疗的潜在用途。

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