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

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...

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Autores principales: Liu, Changkun, Chen, Zhouguang, Fang, Jianzheng, Xu, Aiming, Wang, Zengjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842524/
http://dx.doi.org/10.21037/tau.2016.s144
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author Liu, Changkun
Chen, Zhouguang
Fang, Jianzheng
Xu, Aiming
Wang, Zengjun
author_facet Liu, Changkun
Chen, Zhouguang
Fang, Jianzheng
Xu, Aiming
Wang, Zengjun
author_sort Liu, Changkun
collection PubMed
description 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.
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spelling pubmed-48425242016-05-09 AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation Liu, Changkun Chen, Zhouguang Fang, Jianzheng Xu, Aiming Wang, Zengjun Transl Androl Urol Printed Abstracts 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. AME Publishing Company 2016-04 /pmc/articles/PMC4842524/ http://dx.doi.org/10.21037/tau.2016.s144 Text en 2016 Translational Andrology and Urology. All rights reserved.
spellingShingle Printed Abstracts
Liu, Changkun
Chen, Zhouguang
Fang, Jianzheng
Xu, Aiming
Wang, Zengjun
AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
title AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
title_full AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
title_fullStr AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
title_full_unstemmed AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
title_short AB144. H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
title_sort ab144. h19-derived mir-675 contributes to bladder cancer cell proliferation by regulating p53 activation
topic Printed Abstracts
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4842524/
http://dx.doi.org/10.21037/tau.2016.s144
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