Hsa-miR-429 promotes bladder cancer cell proliferation via inhibiting CDKN2B

// Jiangeng Yang 1, 2 , Yuchen Liu 1, 2 , Anbang He 1, 2, 3 , Yuhan Liu 1 , Jianting Wu 1 , Xinhui Liao 1 , Zhaojie Lv 1 , Feng Wang 1 and Hongbing Mei 1, 2 1 Department of Urology, Shenzhen Second People’s Hospital, Clinical Institute of Guangzhou Medical University, Shenzhen, China 2 Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China 3 Anhui Medical University, Anhui, China Correspondence to: Hongbing Mei, email: hbmei68@163.com Keywords: microRNA, urothelial carcinoma, cyclin-dependent kinase inhibitor 2B Received: December 28, 2016     Accepted: July 06, 2017     Published: August 03, 2017 ABSTRACT Background and Objectives: Hsa-miR-429 is increased in bladder cancer. Its roles in bladder cancer are poorly understood. Methods: The expression levels of hsa-miR-429 and cyclin-dependent kinase inhibitor 2B (CDKN2B) were determined using Real-Time qPCR in a total of 50 patients with bladder cancer. Bladder cancer T24 and 5637 cells were transfected CDKN2B siRNA or hsa-miR-429 mimic. CDKN2B expression levels after transfection were detected by Real-Time qPCR and Western blot assay respectively. Binding sites between hsa-miR-429 and 3’-untranslated region of CDKN2B were confirmed by Dual luciferase reporter assay. Cell proliferation was evaluated using MTT and EdU assays. Cell apoptosis was determined using ELISA assay. Results: Higher hsa-miR-429 expression levels were associated with higher tumor grade and stage. All patients with low hsa-miR-429 expression survived 5 years, while with high hsa-miR-429 expression, only 58% survived. Hsa-miR-429 and CDKN2B were inversely expressed in bladder cancer. Hsa-miR-429 mimic decreased the expression of CDKN2B at both mRNA and protein levels. The binding site was confirmed between hsa-miR-429 and 3’-untranslated region of CDKN2B. Up-regulation of hsa-miR-429 or down-regulation of CDKN2B promoted cell growth and decreased apoptosis. Conclusions: Our data suggest a mechanism for hsa-miR-429 to play oncogenic roles via inhibiting CDKN2B.