微小 RNA-375 在胃癌中下调,并通过靶向 PDK1 和 14-3-3zeta 调节细胞存活。
MicroRNA-375 is downregulated in gastric carcinomas and regulates cell survival by targeting PDK1 and 14-3-3zeta.
机构信息
Department of Molecular Pathology, Faculty of Medicine and Institute of Scientific Research, Oita University, Oita, Japan.
出版信息
Cancer Res. 2010 Mar 15;70(6):2339-49. doi: 10.1158/0008-5472.CAN-09-2777. Epub 2010 Mar 9.
We investigated expression profiles of microRNA (miRNA) in gastric carcinomas by use of a miRNA microarray platform covering a total of 470 human miRNAs. We identified 39 differentially expressed miRNAs in gastric carcinoma, of which six were significantly downregulated and the other 33 were upregulated. We found that miRNA-375 (miR-375) was the most downregulated and that its ectopic expression in gastric carcinoma cells markedly reduced cell viability via the caspase-mediated apoptosis pathway. Interestingly, we found that expression of miR-375 inhibited expression of PDK1, which is a direct target of miR-375, followed by suppression of Akt phosphorylation. Further analysis by gene expression microarray revealed that 14-3-3zeta, a potent antiapoptotic gene, was significantly downregulated at both the mRNA and protein levels in cells transfected with miR-375. The activity of a luciferase reporter containing the miR-375 binding sequence at the 3' untranslated region (UTR) of 14-3-3zeta mRNA was repressed by the ectopic expression of miR-375, suggesting that miR-375 targets the 3' UTR of 14-3-3zeta. In addition, knockdown of either PDK1 or 14-3-3zeta in gastric carcinoma cells induced caspase activation, which was also observed in miR-375-transfected cells, suggesting that miR-375 may exert its proapoptotic function, at least in part, through the downregulation of PDK1 and 14-3-3zeta. Taken together, we propose that miR-375 is a candidate tumor suppressor miRNA in gastric carcinoma.
我们使用 miRNA 微阵列平台调查了胃癌中 microRNA (miRNA) 的表达谱,该平台总共涵盖了 470 个人类 miRNA。我们在胃癌中鉴定出 39 个差异表达的 miRNA,其中 6 个显著下调,另外 33 个上调。我们发现 miRNA-375 (miR-375) 下调最显著,其在胃癌细胞中的异位表达通过半胱氨酸天冬氨酸蛋白酶介导的凋亡途径显著降低细胞活力。有趣的是,我们发现 miR-375 的表达抑制了 PDK1 的表达,PDK1 是 miR-375 的直接靶标,随后抑制 Akt 磷酸化。通过基因表达微阵列的进一步分析显示,14-3-3zeta,一种有效的抗凋亡基因,在转染 miR-375 的细胞中在 mRNA 和蛋白水平上均显著下调。包含 14-3-3zeta mRNA 3'非翻译区 (UTR) 中 miR-375 结合序列的荧光素酶报告基因的活性被 miR-375 的异位表达抑制,表明 miR-375 靶向 14-3-3zeta 的 3'UTR。此外,在胃癌细胞中敲低 PDK1 或 14-3-3zeta 诱导半胱氨酸天冬氨酸蛋白酶激活,这也在 miR-375 转染细胞中观察到,表明 miR-375 可能通过下调 PDK1 和 14-3-3zeta 来发挥其促凋亡功能,至少部分如此。总之,我们提出 miR-375 是胃癌中的候选肿瘤抑制 miRNA。