Suppr超能文献

环状PIP5K1A作为一种竞争性内源性RNA,通过调控miR-661/IGFBP5信号通路促进卵巢癌进展。

circPIP5K1A serves as a competitive endogenous RNA contributing to ovarian cancer progression via regulation of miR-661/IGFBP5 signaling.

作者信息

Sun Yi, Li Xue, Chen Aozheng, Shi Weihui, Wang Lei, Yi Ruhai, Qiu Jin

机构信息

Department of Obstetrics and Gynecology, Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Department of Interventional & Vascular Surgery, Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.

出版信息

J Cell Biochem. 2019 Dec;120(12):19406-19414. doi: 10.1002/jcb.29055. Epub 2019 Aug 26.

Abstract

Increasing evidence demonstrates the crucial regulatory functions of circular RNAs in different cancer types. The major aim of the current study was to establish functions of circPIP5K1A during ovarian cancer. Our results showed an increased expression of circPIP5K1A in both ovarian cancers and cell lines, which was associated with poor prognosis. In functional analyses, downregulation of circPIP5K1A suppressed ovarian cancer cell migration, proliferation, and invasion in vitro. The miR-661 was indicated as a target of circPIP5K1A and insulin-like growth factor-binding protein 5 (IGFBP5) as a target of miR-661. circPIP5K1A silencing triggered downregulation of IGFBP5 through inducing an increase in miR-66 levels, as determined by the luciferase reporter assay. Data from cell counting kit-8, colony formation, wound healing, and Transwell assays showed that overexpression of IGFBP5 effectively reversed the circPIP5K1A depletion effects. The results collectively indicated that circPIP5K1A contributed to ovarian cancer progression via targeting the miR-661/IGFBP5 axis, supporting its utility as a candidate target for therapy of the disease.

摘要

越来越多的证据表明环状RNA在不同癌症类型中具有关键的调控功能。本研究的主要目的是确定circPIP5K1A在卵巢癌中的作用。我们的结果显示,circPIP5K1A在卵巢癌组织和细胞系中均表达增加,且与预后不良相关。在功能分析中,circPIP5K1A的下调抑制了卵巢癌细胞在体外的迁移、增殖和侵袭。miR-661被证实为circPIP5K1A的靶标,胰岛素样生长因子结合蛋白5(IGFBP5)为miR-661的靶标。荧光素酶报告基因检测结果表明,circPIP5K1A沉默通过诱导miR-66水平升高,引发IGFBP5下调。细胞计数试剂盒-8、集落形成、伤口愈合及Transwell实验数据表明,IGFBP5过表达有效逆转了circPIP5K1A缺失效应。这些结果共同表明,circPIP5K1A通过靶向miR-661/IGFBP5轴促进卵巢癌进展,支持其作为该疾病治疗候选靶点的效用。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验