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TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells
Aberrant expression of microRNAs hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resistance. However, mechanisms underlying the role of mcroRNAs in glioblastoma cell growth and apoptosis are not fully understood. In this study, we report that miR-503...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599596/ https://www.ncbi.nlm.nih.gov/pubmed/28912531 http://dx.doi.org/10.1038/s41598-017-11885-8 |
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author | Guo, Pin Yu, Yanan Li, Huanting Zhang, Daoxiang Gong, Anjing Li, Shifang Liu, Wei Cheng, Lei Qiu, Yongming Yao, Weicheng Li, Luo Feng, Yugong |
author_facet | Guo, Pin Yu, Yanan Li, Huanting Zhang, Daoxiang Gong, Anjing Li, Shifang Liu, Wei Cheng, Lei Qiu, Yongming Yao, Weicheng Li, Luo Feng, Yugong |
author_sort | Guo, Pin |
collection | PubMed |
description | Aberrant expression of microRNAs hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resistance. However, mechanisms underlying the role of mcroRNAs in glioblastoma cell growth and apoptosis are not fully understood. In this study, we report that miR-503 is overexpressed in glioblastoma tissue compared with normal human brain tissue. Mechanistically, miR-503 can be induced by TGF-β1 at the transcriptional level by binding the smad2/3 binding elements in the promoter. Ectopic overexpression of miR-503 promotes cell growth and inhibits apoptosis by targeting PDCD4. In contrast, inhibition of miR-503 reduces cell growth. Furthermore, miR-503 inhibitor augments the growth inhibitory effect of temozolomide in glioblastoma cells. These results establish miR-503 as a promising molecular target for glioblastoma therapy. |
format | Online Article Text |
id | pubmed-5599596 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-55995962017-09-15 TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells Guo, Pin Yu, Yanan Li, Huanting Zhang, Daoxiang Gong, Anjing Li, Shifang Liu, Wei Cheng, Lei Qiu, Yongming Yao, Weicheng Li, Luo Feng, Yugong Sci Rep Article Aberrant expression of microRNAs hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resistance. However, mechanisms underlying the role of mcroRNAs in glioblastoma cell growth and apoptosis are not fully understood. In this study, we report that miR-503 is overexpressed in glioblastoma tissue compared with normal human brain tissue. Mechanistically, miR-503 can be induced by TGF-β1 at the transcriptional level by binding the smad2/3 binding elements in the promoter. Ectopic overexpression of miR-503 promotes cell growth and inhibits apoptosis by targeting PDCD4. In contrast, inhibition of miR-503 reduces cell growth. Furthermore, miR-503 inhibitor augments the growth inhibitory effect of temozolomide in glioblastoma cells. These results establish miR-503 as a promising molecular target for glioblastoma therapy. Nature Publishing Group UK 2017-09-14 /pmc/articles/PMC5599596/ /pubmed/28912531 http://dx.doi.org/10.1038/s41598-017-11885-8 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Guo, Pin Yu, Yanan Li, Huanting Zhang, Daoxiang Gong, Anjing Li, Shifang Liu, Wei Cheng, Lei Qiu, Yongming Yao, Weicheng Li, Luo Feng, Yugong TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells |
title | TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells |
title_full | TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells |
title_fullStr | TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells |
title_full_unstemmed | TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells |
title_short | TGF-β1-induced miR-503 controls cell growth and apoptosis by targeting PDCD4 in glioblastoma cells |
title_sort | tgf-β1-induced mir-503 controls cell growth and apoptosis by targeting pdcd4 in glioblastoma cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599596/ https://www.ncbi.nlm.nih.gov/pubmed/28912531 http://dx.doi.org/10.1038/s41598-017-11885-8 |
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