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microRNA-203 suppresses bladder cancer development by repressing bcl-w expression.

Authors :
Bo, Juanjie
Yang, Guoliang
Huo, Kailing
Jiang, Haifeng
Zhang, Lianhua
Liu, Dongming
Huang, Yiran
Source :
FEBS Journal. Mar2011, Vol. 278 Issue 5, p786-792. 7p.
Publication Year :
2011

Abstract

It is increasingly clear that microRNAs (miRNAs) play an important role in many diseases, including tumorigenesis. However, the mechanisms by which miRNAs regulate bladder cancer development remain poorly understood. Here, we evaluated the expression of microRNA-203 (miR-203) in bladder cancer tissues using real-time PCR, and defined the target genes and biologically functional effect using luciferase reporter assay, flow cytometry and western blot analysis. We first verified that the expression of miR-203 was decreased in bladder cancer tissues. Moreover, ectopic expression of miR-203 promoted the apoptosis of human bladder cancer cell lines and inhibited cell proliferation, whereas its depletion increased cell growth. We further verified that miR-203 directly targeted 3′-untranslated region of the bcl-w gene, and decreased its expression in vitro and in vivo. Western blot analysis also showed that the expression level of miR-203 was negatively correlated with bcl-w level in tumor tissues. These data suggest an important role for miR-203 in the molecular etiology of bladder cancer and implicate the potential application of miR-203 in bladder cancer therapy. We verified that the expression of microRNA-203 (miR-203) was decreased in bladder cancer tissues. Moreover, ectopic expression of miR-203 promoted the apoptosis of human bladder cancer cell lines. The expression of miR-203 decreased both in vitro and in vivo. Western blot analysis showed that the expression level of miR-203 was negatively correlated with bcl-w level in tumor tissues. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
1742464X
Volume :
278
Issue :
5
Database :
Academic Search Index
Journal :
FEBS Journal
Publication Type :
Academic Journal
Accession number :
58467905
Full Text :
https://doi.org/10.1111/j.1742-4658.2010.07997.x