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

• Published in: Journal of cellular biochemistry 2019-12, Vol.120 (12), p.19406-19414
• Main Authors: Sun, Yi, Li, Xue, Chen, Aozheng, Shi, Weihui, Wang, Lei, Yi, Ruhai, Qiu, Jin
• Format: Article
• Language: English
• Subjects: Cancer; Cell adhesion & migration; Cell migration; circPIP5K1A; Depletion; Growth factors; IGFBP5; Insulin; Insulin-like growth factor-binding protein 5; invasion; miR‐661; Ovarian cancer; proliferation; Ribonucleic acid; RNA; Wound healing
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.29055

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. 1. circPIP5K1A contributed to ovarian cancer progression through targeting the miR‐661/IGFBP5 axis. 2. circPIP5K1A silencing triggered downregulation of IGFBP5 by promotion miR‐66 expression.