Cargando…
H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation
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. In this study, we first evaluated the expression of miR-675 in bladder cancer t...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841850/ https://www.ncbi.nlm.nih.gov/pubmed/26198047 http://dx.doi.org/10.1007/s13277-015-3779-2 |
_version_ | 1782428435287638016 |
---|---|
author | Liu, Changkun Chen, Zhouguang Fang, Jianzheng Xu, Aiming Zhang, Wei Wang, Zengjun |
author_facet | Liu, Changkun Chen, Zhouguang Fang, Jianzheng Xu, Aiming Zhang, Wei Wang, Zengjun |
author_sort | Liu, Changkun |
collection | PubMed |
description | 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. 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. 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. 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-4841850 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-48418502016-05-16 H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation Liu, Changkun Chen, Zhouguang Fang, Jianzheng Xu, Aiming Zhang, Wei Wang, Zengjun Tumour Biol Original Article 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. 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. 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. 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. Springer Netherlands 2015-07-22 /pmc/articles/PMC4841850/ /pubmed/26198047 http://dx.doi.org/10.1007/s13277-015-3779-2 Text en © The Author(s) 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Original Article Liu, Changkun Chen, Zhouguang Fang, Jianzheng Xu, Aiming Zhang, Wei Wang, Zengjun H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
title | H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
title_full | H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
title_fullStr | H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
title_full_unstemmed | H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
title_short | H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
title_sort | h19-derived mir-675 contributes to bladder cancer cell proliferation by regulating p53 activation |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841850/ https://www.ncbi.nlm.nih.gov/pubmed/26198047 http://dx.doi.org/10.1007/s13277-015-3779-2 |
work_keys_str_mv | AT liuchangkun h19derivedmir675contributestobladdercancercellproliferationbyregulatingp53activation AT chenzhouguang h19derivedmir675contributestobladdercancercellproliferationbyregulatingp53activation AT fangjianzheng h19derivedmir675contributestobladdercancercellproliferationbyregulatingp53activation AT xuaiming h19derivedmir675contributestobladdercancercellproliferationbyregulatingp53activation AT zhangwei h19derivedmir675contributestobladdercancercellproliferationbyregulatingp53activation AT wangzengjun h19derivedmir675contributestobladdercancercellproliferationbyregulatingp53activation |