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首页> 外文期刊>The FEBS journal >MicroRNA-23b mediates urokinase and c-met downmodulation and a decreased migration of human hepatocellular carcinoma cells
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MicroRNA-23b mediates urokinase and c-met downmodulation and a decreased migration of human hepatocellular carcinoma cells

机译：MicroRNA-23b介导尿激酶和c-met下调以及人类肝癌细胞的迁移减少

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摘要

Urokinase-type plasminogen activator (uPA) and c-met play a major role in cancer invasion and metastasis. Evidence has suggested that uPA and c-met overexpression may be coordinated in human hepatocellular carcinoma (HCC). In the present study, to understand whether the expression of these genes might be coregulated by specific microRNAs (miRs) in human cells, we predicted that Homo sapiens microRNA-23b could recognize two sites in the 3'-UTR of uPA and four sites in the c-met 3'-UTR by the algorithm pictar. The miR-23b expression analysis in human tumor and normal cells revealed an inverse trend with uPA and c-met expression, indicating that uPA and c-met negative regulation might depend on miR-23b expression. Transfection of miR-23b molecules in HCC cells (SKHep1C3) led to inhibition of protein expression of the target genes and caused a decrease in cell migration and proliferation capabilities. Furthermore, anti-miR-23b transfection in human normal AB2 dermal fibroblasts upregulated the expression of endogenous uPA and c-met. Cotransfection experiments in HCC cells of the miR-23b with pGL4.71 Renilla luciferase reporter gene constructs, containing the putative uPA and c-met 3'-UTR target sites, and with the pGL3 firefly luciferase-expressing vector showed a decrease in the relative luciferase activity. This would indicate that miR-23b can recognize target sites in the 3'-UTR of uPA and of c-met mRNAs and translationally repress the expression of uPA and c-met in HCC cells. The evidence obtained shows that overexpression of miR-23b leads to uPA and c-met downregulation and to decreased migration and proliferation abilities of HCC cells.
机译：尿激酶型纤溶酶原激活剂（uPA）和c-met在癌症侵袭和转移中起主要作用。有证据表明，uPA和c-met过表达可能在人类肝细胞癌（HCC）中得到协调。在本研究中，为了了解这些基因的表达是否可能被人类细胞中的特定microRNA（miR）调控，我们预测智人microRNA-23b可以识别uPA 3'-UTR中的两个位点和人类中的四个位点。算法图片显示c-met 3'-UTR。在人肿瘤和正常细胞中的miR-23b表达分析显示uPA和c-met表达呈逆趋势，表明uPA和c-met负调控可能取决于miR-23b表达。 miR-23b分子在HCC细胞（SKHep1C3）中的转染导致靶基因蛋白表达受到抑制，并导致细胞迁移和增殖能力下降。此外，在人正常AB2真皮成纤维细胞中进行抗miR-23b转染可上调内源性uPA和c-met的表达。在miR-23b的HCC细胞中与含有假定的uPA和c-met 3'-UTR目标位点的pGL4.71 Renilla荧光素酶报道基因基因构建体以及与表达pGL3萤火虫荧光素酶的载体共转染实验显示相对萤光素酶活性。这表明miR-23b可以识别uPA和c-met mRNA的3'-UTR中的靶位点，并翻译抑制HCC细胞中uPA和c-met的表达。获得的证据表明，miR-23b的过表达导致uPA和c-met下调，并导致HCC细胞迁移和增殖能力降低。

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