miR-92a promotes hepatocellular carcinoma cells proliferation and invasion by FOXA2 targeting.
miR-92a promotes hepatocellular carcinoma cells proliferation and invasion by FOXA2 targeting.
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miR-92a促进肝细胞癌细胞的增殖和FOXA2靶向侵袭。
DOI：
10.22038/ijbms.2017.9010
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发表时间：
2017-07
影响因子：
2.2
通讯作者：
Xie C
中科院分区：
文献类型：
--
作者：
Wang L;Wu J;Xie C
MicroRNA (miRNA) 被认为是肝细胞癌细胞 (HCC) 中基因表达的强大转录后调节因子。然而，miR-92a在HCC中的功能仍不清楚。使用 qRT-PCR 评估人 HCC 细胞系中 miR-92a 的表达。采用MTT法和Transwell法检测miR-92a在HepG2和Huh7细胞中的功能。使用生物信息学分析和荧光素酶报告基因测定来验证 FOXA2 作为 miR-92a 的直接靶基因。一致地，通过体外增殖和侵袭分析检查了 miR-92a 调节 FOXA2 的生物学结果。在这里，我们检测到与正常人肝细胞L02细胞相比，miR-92a在人HCC细胞系（例如HepG2、Huh7和Hep3B）中表达更高。 miR-92a的过表达显着增加了细胞的生长和侵袭能力，而miR-92a的敲低则显着抑制了细胞的生长和侵袭能力。我们发现 miR-92a 在 FOXA2 的 3'-UTR 中具有特定的靶向位点。通过在HepG2细胞或Huh7细胞中过表达miR-92a，FOXA2的表达被显着抑制。我们证明 miR-92a 可能在 HCC 增殖和侵袭中发挥关键作用，并可能通过抑制 FOXA2 作为新的治疗靶点。
MicroRNAs (miRNAs) are considered as powerful, post-transcriptional regulators of gene expression in hepatocellular carcinoma cells (HCC). However, the function of miR-92a is still unclear in HCC. Expression of miR-92a in human HCC cell lines was evaluated using qRT-PCR. MTT assay and transwell assay were used to examine the function of miR-92a in HepG2 and Huh7 cells. Bioinformatic analyses and luciferase reporter assays were used to validate FOXA2 as a direct target gene of miR-92a. Consistently, the biological outcome of miR-92a on regulating FOXA2 was examined by proliferation and invasion analysis in vitro. Here, we detected the higher expression of miR-92a in human HCC cell lines, such as HepG2, Huh7 and Hep3B, compared with the normal human hepatocyte L02 cells. Overexpression of miR-92a significantly increased cell growth and invasion ability, while the knockdown of miR-92a could remarkably inhibit the growth and invasion possibility. We identified that miR-92a has specific targeting sites in the 3’-UTR of the FOXA2. By overexpressing miR-92a in HepG2 cells or Huh7 cells, the expression of FOXA2 was remarkably repressed. We demonstrated that miR-92a may play a critical role in HCC proliferation and invasion and may serve as a novel therapeutic target by the repression of FOXA2.