Circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene

Abstract

Background: Cervical cancer (CC) is a highly malignant tumor. Evolving researches on CC have unveiled a concept that circRNA exerts important roles in CC progression. In this study, we mainly explored the role of a novel circRNA, circ_0084927, and its regulatory network in the development of CC. Methods: qRT-PCR was applied to evaluate the expression of circ_0084927, miR-1179 and CDK2 mRNA in CC tissues and cells. Dual-luciferase reporting experiments and RNA immunoprecipitation (RIP) assay were conducted to validate the target relationship of miR-1179 with circ_0084927 and CDK2 mRNA. CCK-8 and BrdU assay was used to evaluate CC cell proliferation. The adhesion and apoptosis phenotypes of CC cells were measured by cell-matrix adhesion and caspase 3 activation assay. Flow cytometry was employed to detect CC cell cycle. Results: Our results indicated that circ_0084927 was up-regulated in CC tissues and cells, and circ_0084927 silence inhibited CC cell proliferation and adhesion, while facilitating apoptosis as well as triggering cell cycle arrest. On the other hand, miR-1179 down-regulation appeared in CC tissues. Additionally, circ_0084927 abolished miR-1179’s inhibitory effects on cell proliferation and adhesion. Our study showed that CDK2 was up-regulated in CC tissues and played a cancer-promoting role. Furthermore, miR-1179 directly targeted CDK2, thereby inhibiting CDK2’s promotion on the malignant phenotypes of CC cells. circ_0084927 revoked the inhibitory effect of miR-1179 on CDK2 by sponging miR-1179. Conclusion: Circ_0084927 promoted cervical carcinogenesis by sequestering miR-1179 that directly targeted CDK2. Our results shed light on the circ_0084927/miR-1179/CDK2 regulatory network that strengthened CC aggressiveness, providing novel candidate targets for CC treatment.