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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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2016
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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. |
format | Online Article Text |
id | pubmed-4842524 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
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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