Oncotarget

Research Papers:

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

Jiangeng Yang, Yuchen Liu, Anbang He, Yuhan Liu, Jianting Wu, Xinhui Liao, Zhaojie Lv, Feng Wang and Hongbing Mei _

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Oncotarget. 2017; 8:68721-68729. https://doi.org/10.18632/oncotarget.19878

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Abstract

Jiangeng Yang1,2, Yuchen Liu1,2, Anbang He1,2,3, Yuhan Liu1, Jianting Wu1, Xinhui Liao1, Zhaojie Lv1, Feng Wang1 and Hongbing Mei1,2

1Department of Urology, Shenzhen Second People’s Hospital, Clinical Institute of Guangzhou Medical University, Shenzhen, China

2Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People’s Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, China

3Anhui 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.


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