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