Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer

MicroRNA-30c (miR-30c) has been reported to be a tumour suppressor in endometrial cancer (EC). We demonstrate that miR-30c is down-regulated in EC tissue and is highly expressed in estrogen receptor (ER)-negative HEC-1-B cells. MiR-30c directly inhibits MTA-1 expression and functions as a tumour sup...

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Autores principales: Kong, Xiangyi, Xu, XiaoFeng, Yan, Yuhua, Guo, Feifei, Li, Jian, Hu, Yali, Zhou, Huaijun, Xun, Qingying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940948/
https://www.ncbi.nlm.nih.gov/pubmed/24595016
http://dx.doi.org/10.1371/journal.pone.0090810
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author Kong, Xiangyi
Xu, XiaoFeng
Yan, Yuhua
Guo, Feifei
Li, Jian
Hu, Yali
Zhou, Huaijun
Xun, Qingying
author_facet Kong, Xiangyi
Xu, XiaoFeng
Yan, Yuhua
Guo, Feifei
Li, Jian
Hu, Yali
Zhou, Huaijun
Xun, Qingying
author_sort Kong, Xiangyi
collection PubMed
description MicroRNA-30c (miR-30c) has been reported to be a tumour suppressor in endometrial cancer (EC). We demonstrate that miR-30c is down-regulated in EC tissue and is highly expressed in estrogen receptor (ER)-negative HEC-1-B cells. MiR-30c directly inhibits MTA-1 expression and functions as a tumour suppressor via the miR-30c-MTA-1 signalling pathway. Furthermore, miR-30c is decreased upon E(2) treatment in both ER-positive Ishikawa and ER-negative HEC-1-B cells. Taken together, our results suggest that miR-30c is an important deregulated miRNA in EC and might serve as a potential biomarker and novel therapeutic target for EC.
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spelling pubmed-39409482014-03-06 Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer Kong, Xiangyi Xu, XiaoFeng Yan, Yuhua Guo, Feifei Li, Jian Hu, Yali Zhou, Huaijun Xun, Qingying PLoS One Research Article MicroRNA-30c (miR-30c) has been reported to be a tumour suppressor in endometrial cancer (EC). We demonstrate that miR-30c is down-regulated in EC tissue and is highly expressed in estrogen receptor (ER)-negative HEC-1-B cells. MiR-30c directly inhibits MTA-1 expression and functions as a tumour suppressor via the miR-30c-MTA-1 signalling pathway. Furthermore, miR-30c is decreased upon E(2) treatment in both ER-positive Ishikawa and ER-negative HEC-1-B cells. Taken together, our results suggest that miR-30c is an important deregulated miRNA in EC and might serve as a potential biomarker and novel therapeutic target for EC. Public Library of Science 2014-03-03 /pmc/articles/PMC3940948/ /pubmed/24595016 http://dx.doi.org/10.1371/journal.pone.0090810 Text en © 2014 Kong et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Kong, Xiangyi
Xu, XiaoFeng
Yan, Yuhua
Guo, Feifei
Li, Jian
Hu, Yali
Zhou, Huaijun
Xun, Qingying
Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer
title Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer
title_full Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer
title_fullStr Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer
title_full_unstemmed Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer
title_short Estrogen Regulates the Tumour Suppressor MiRNA-30c and Its Target Gene, MTA-1, in Endometrial Cancer
title_sort estrogen regulates the tumour suppressor mirna-30c and its target gene, mta-1, in endometrial cancer
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940948/
https://www.ncbi.nlm.nih.gov/pubmed/24595016
http://dx.doi.org/10.1371/journal.pone.0090810
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