Inhibition of miR-96 expression reduces cell proliferation and clonogenicity of HepG2 hepatoma cells
Inhibition of miR-96 expression reduces cell proliferation and clonogenicity of HepG2 hepatoma cells
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抑制 miR-96 表达可降低 HepG2 肝癌细胞的细胞增殖和克隆形成
DOI：
10.3892/or.2012.2138
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发表时间：
2013-02-01
期刊：
影响因子：
4.2
通讯作者：
Lin, Jusheng
中科院分区：
文献类型：
--
作者：
Xu, Dong;He, Xingxing;Lin, Jusheng
microRNAs （miRNAs）是基因表达的负调控因子，可以作为肿瘤抑制因子或致癌基因。几种mirna与肝细胞癌（HCC）的发展有关。miR-96与细胞增殖和克隆原性密切相关。miR-96的上调已经在各种类型的癌症中被观察到。然而，miR-96在肝癌发生中的生物学功能在很大程度上仍然未知。在本研究中，我们证实miR-96在HCC中表达上调，抑制miR-96可显著抑制HCC细胞增殖和集落形成。当miR-96在HCC细胞中被抑制时，forkhead box 01 （FOXO1）和forkhead box O3a （FOXO3a）的表达水平上调，FOXO1和FOXO3a的抑制促进了HCC细胞的增殖和集落形成。总的来说，这些数据揭示了miR-96对肝癌发生的重要贡献，并提示FOXO1和FOXO3a失调在这一过程中起作用。因此，使用miR-96的合成抑制剂可能是一种治疗HCC的有希望的方法。
microRNAs (miRNAs) are negative regulators of gene expression and can function as tumor suppressors or oncogenes. Several miRNAs are associated with the development of hepatocellular carcinoma (HCC). miR-96 has been closely associated with cell proliferation and clonogenicity. Upregulation of miR-96 has been observed in various types of cancer. However, the biological function of miR-96 in hepatocarcinogenesis remains largely unknown. In this study, we demonstrated that miR-96 was upregulated in HCC and inhibition of miR-96 significantly suppressed HCC cell proliferation and colony formation. The expression levels of forkhead box 01 (FOXO1) and forkhead box O3a (FOXO3a) were upregulated when miR-96 was inhibited in HCC cells and the inhibition of FOXO1 and FOXO3a promoted HCC cell proliferation and colony formation. Collectively, these data reveal an important contribution of miR-96 to hepatocarcinogenesis and suggest a role for FOXO1 and FOXO3a dysregulation in this process. Thus, the use of a synthetic inhibitor of miR-96 may be a promising approach for the treatment of HCC.