To investigate the action mechanism of lncRNA CDKN2B-AS1/hsa-miR-134-5p/CCND1 axis in cervical cancer based on bioinformatics

Abstract Objectives Cervical cancer (CC) is a malignant tumor that poses a serious threat to women’s lives and has a complex pathogenesis. This study aims to investigate the mechanism underlying the lncRNA CDKN2B-AS1 in CC. Methods The expression of CDKN2B-AS1, hsa-miR-134-5p, and CCND1 was detected by RT-qPCR and western blotting, and their targeted regulatory relationships were verified by dual-luciferase reporter assay and overexpression/knockdown assay. CCK-8, Transwell, and Annexin V-FITC/PI staining experiments were used to assess the proliferation, migration, invasion and apoptosis of CC cells (HeLa and SiHa), respectively. The Kaplan-Meier survival curve was used to evaluate the clinical value of CDKN2B-AS1 in CC. Results CDKN2B-AS1, CCND1 were high-expressed, and hsa-miR-134-5p was low-expressed in CC cells and tissues. Silencing CDKN2B-AS1 significantly inhibited the growth and metastasis of HeLa and SiHa cells, and induced their apoptosis. The overall survival time of CC patients with high CDKN2B-AS1 was shorter (log rank p<0.05). Hsa-miR-134-5p mimic attenuated the luciferase activity of cells transfected with wild-type CDKN2B/CCND1 luciferase vector. Overexpression of CDKN2B-AS1 decreased the intracellular level of hsa-miR-134-5p, while its knockdown was inverse. The inhibition of hsa-miR-134-5p promoted CCND1 expression. Conclusions High CDKN2B-AS1 level predicted a poor prognosis of CC patients, and it promoted CC development by down-regulating hsa-miR-134-5p to enhance CCND1 expression.