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首页> 外文期刊>Journal of cellular biochemistry. >MiR-17-5p Up-Regulates YES1 to Modulate the Cell Cycle Progression and Apoptosis in Ovarian Cancer Cell Lines
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MiR-17-5p Up-Regulates YES1 to Modulate the Cell Cycle Progression and Apoptosis in Ovarian Cancer Cell Lines

机译：MiR-17-5p上调YES1以调节卵巢癌细胞系中的细胞周期进程和凋亡

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摘要

MicroRNAs (miRNAs) are small, non-coding RNAs that participate in the regulation of gene expression. Although many studies have demonstrated the involvement of miR-17-5p in different cancers, little is known to its function in ovarian cancer. In this study, we demonstrated that overexpression of miR-17-5p was able to enhance cell proliferation by promoting G1/S transition of the cell cycle and suppressing apoptosis in ES-2 and OVCAR3 cell lines, whereas inhibition of miR-17-5p yielded the reverse phenotype. YES1 was identified as a novel target gene of miR-17-5p. Moreover, miR-17-5p was found to directly bind to the 30UTR of YES1 mRNA and up-regulated its expression. Furthermore, knockdown of YES1 led to the suppression of proliferation and induced cell cycle arrest in ES-2 and OVCAR3 cells. Ectopic expression of YES1 was able to reverse the effects of miR-17-5p inhibition. Collectively, our results indicated that miR-17-5p might play a role in human ovarian cancer by up-regulating YES1 expression. (C) 2015 Wiley Periodicals, Inc.
机译：微小RNA（miRNA）是小的非编码RNA，参与基因表达的调节。尽管许多研究表明miR-17-5p参与了不同的癌症，但对其在卵巢癌中的功能知之甚少。在这项研究中，我们证明了miR-17-5p的过表达能够通过促进细胞周期的G1 / S过渡和抑制ES-2和OVCAR3细胞系的凋亡来增强细胞增殖，而抑制miR-17-5p产生反向表型。 YES1被确定为miR-17-5p的新型靶基因。此外，发现miR-17-5p直接与YES1 mRNA的30UTR结合并上调其表达。此外，敲低YES1可导致ES-2和OVCAR3细胞的增殖受到抑制并诱导细胞周期停滞。 YES1的异位表达能够逆转miR-17-5p抑制作用。总的来说，我们的结果表明miR-17-5p可能通过上调YES1表达在人类卵巢癌中发挥作用。 （C）2015威利期刊公司

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