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miR-661 通过抑制 INPP5J 表达促进人卵巢癌细胞的增殖。

MiR-661 contributed to cell proliferation of human ovarian cancer cells by repressing INPP5J expression.

机构信息

Department of Obstetrics and Gynecology, General Hospital of Jinan Military Command, Shandong 250031, People's Republic of China.

Department of Medical Information, General Hospital of Jinan Military Command. Shandong 250031, People's Republic of China.

出版信息

Biomed Pharmacother. 2015 Oct;75:123-8. doi: 10.1016/j.biopha.2015.07.023. Epub 2015 Aug 15.

Abstract

Accumulating evidence has emerged important roles for microRNAs (miRNAs) participating in oncogenesis and growth of various cancers. We hypothesized that miR-661 played an important role in cell growth of ovarian cancer. Here, we found miR-661 was upregulated in human ovarian cancer cell lines and clinical tumor tissues. Our results revealed that miR-661 directly targeted INPP5J, thereby acting as tumor promoter in ovarian cancer cells by blocking cell proliferation. Importantly, we identified miR-661 as a positive regulator of INPP5J-induced AKT pathway. Taken together, our study sheds light onto the role of miR-661 as tumor promoter by targeting the INPP5J gene, and then promoting cell proliferation of ovarian cancer.

摘要

越来越多的证据表明,microRNAs(miRNAs)在各种癌症的发生和生长中起着重要作用。我们假设 miR-661 在卵巢癌细胞的生长中发挥了重要作用。在这里,我们发现 miR-661 在人卵巢癌细胞系和临床肿瘤组织中上调。我们的结果表明,miR-661 直接靶向 INPP5J,从而通过阻断细胞增殖在卵巢癌细胞中充当肿瘤促进剂。重要的是,我们确定 miR-661 是 INPP5J 诱导的 AKT 通路的正调节剂。总之,我们的研究揭示了 miR-661 通过靶向 INPP5J 基因作为肿瘤促进剂的作用,从而促进卵巢癌细胞的增殖。

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