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. found in the lowermost part of the womb. Evolving researchesstudies on CC have unveiled a conceptreported that circRNA exerts important rolesplays a crucial role in CC progression. In this study, we mainly exploredinvestigated the rolemain function of a novel circRNA, circ_0084927, and its regulatory network in theCC 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 wasassays were also used to evaluate CC cell proliferation. The adhesion and apoptosis phenotypes of CC cells were measured byusing 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, and. Findings also revealed that circ_0084927 silence inhibited CC cell proliferation and adhesion, while facilitating apoptosis as well asand triggering cell cycle arrest. On the other handHowever, miR-1179 down-regulation appeared in CC tissues. Additionally,Apart from observing that circ_0084927 abolished miR-1179’s inhibitory effects on cell proliferation and adhesion. Our study showed, it was found that CDK2 was up-regulated in CC tissues and played awas instrumental in cancer-promoting role. Furthermore, 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: Circcirc_0084927 promoted cervical carcinogenesis by sequestering miR-1179 that, which directly targeted CDK2. Our results shed light onalso provided novel candidate targets for CC treatment in that it revealed the circ_0084927/miR-1179/CDK2 regulatory network that strengthened CC aggressiveness, providing novel candidate targets for CC treatment..