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Hsa-miR-429 is increased in bladder cancer. Its roles in bladder cancer are poorly understood. 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. 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. Our data suggest a mechanism for hsa-miR-429 to play oncogenic roles via inhibiting CDKN2B.

Citation

Jiangeng Yang, Yuchen Liu, Anbang He, Yuhan Liu, Jianting Wu, Xinhui Liao, Zhaojie Lv, Feng Wang, Hongbing Mei. Hsa-miR-429 promotes bladder cancer cell proliferation via inhibiting CDKN2B. Oncotarget. 2017 Sep 15;8(40):68721-68729


PMID: 28978151

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