circ-0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene

Abstract

Background: Cervical cancer (CC) is a malignant tumor found in the lowermost part of the womb. Evolving studies on CC have reported that circRNA plays a crucial role in CC progression. In this study, we investigated the main function of a novel circRNA, circ-0084927, and its regulatory network in CC development. 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 assays were also used to evaluate CC cell proliferation. The adhesion and apoptosis phenotypes of CC cells were measured using cell-matrix adhesion and caspase 3 activation assay. Flow cytometry was also employed to detect the CC cell cycle. Results: Our results indicated that circ-0084927 was up-regulated in CC tissues and cells. Findings also revealed that circ-0084927 silence inhibited CC cell proliferation and adhesion while facilitating apoptosis and triggering cell cycle arrest. However, miR-1179 down-regulation appeared in CC tissues. Apart from observing that circ-0084927 abolished miR-1179's inhibitory effects on cell proliferation and adhesion, it was found that CDK2 was up-regulated in CC tissues and was instrumental in cancer promotion. Also observed was that miR-1179 directly targeted CDK2, thereby inhibiting CDK2's promotion on the malignant phenotypes of CC cells. Lastly, results indicated that 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, which directly targeted CDK2. Our results also provided novel candidate targets for CC treatment in that it revealed the circ-0084927/miR-1179/CDK2 regulatory network that strengthened CC aggressiveness.