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Translational Andrology and Urology logoLink to Translational Andrology and Urology
. 2016 Apr;5(Suppl 1):AB144. doi: 10.21037/tau.2016.s144

AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation

Changkun Liu 1, Zhouguang Chen 1, Jianzheng Fang 2, Aiming Xu 2, Zengjun Wang 2
PMCID: PMC4842524

Abstract

Objective

Long noncoding RNA 19 (H19) has been shown to promote bladder cancer cell proliferation and metastasis. However, little is known about how miR-675, mature product of H19, contributes to bladder cancer cell proliferation.

Methods

In this study, we first evaluated the expression of miR-675 in bladder cancer tissues by quantitative real-time PCR (qRT-PCR) and defined its biological functions by flow cytometry and Western blotting.

Results

We found that miR-675 expression levels were remarkably increased in bladder cancer tissues as compared with adjacent noncancerous tissues or normal bladder tissue from health donors; moreover, enhanced miR-675 expression was also observed in bladder cancer cell lines. Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro. Furthermore, overexpression of miR-675 promoted bladder cancer cell proliferation, while suppression of miR-675 induced G1 phase cell cycle arrest and promoted cell apoptosis. Western blotting analysis further identified that miR-675 inhibited p53 activation, decreased the ratio of Bax/Bcl-2 and cyclin D1 expression in bladder cancer cells; those effects may result in the abnormal proliferation of bladder cancer cells.

Conclusions

In conclusion, abnormal enhanced miR-675 expression increases bladder cancer growth by regulating p53 activation, and thus may be helpful in the development of effective treatment strategies for bladder cancer.

Keywords: Bladder cancer, miR-675, proliferation, p53


Articles from Translational Andrology and Urology are provided here courtesy of AME Publications

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