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MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN

BACKGROUND: MicroRNAs are a class of small non-coding RNAs that play an important role in various human tumor initiation and progression by regulating gene expression negatively. The aim of this study was to investigate the effect of miR-214 on cell proliferation, migration and invasion, as well as...

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Autores principales: Yang, Ting-Song, Yang, Xiao-Hu, Wang, Xu-Dong, Wang, Yi-Ling, Zhou, Bo, Song, Zhen-Shun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3716801/
https://www.ncbi.nlm.nih.gov/pubmed/23834902
http://dx.doi.org/10.1186/1475-2867-13-68
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author Yang, Ting-Song
Yang, Xiao-Hu
Wang, Xu-Dong
Wang, Yi-Ling
Zhou, Bo
Song, Zhen-Shun
author_facet Yang, Ting-Song
Yang, Xiao-Hu
Wang, Xu-Dong
Wang, Yi-Ling
Zhou, Bo
Song, Zhen-Shun
author_sort Yang, Ting-Song
collection PubMed
description BACKGROUND: MicroRNAs are a class of small non-coding RNAs that play an important role in various human tumor initiation and progression by regulating gene expression negatively. The aim of this study was to investigate the effect of miR-214 on cell proliferation, migration and invasion, as well as the functional connection between miR-214 and PTEN in gastric cancer. METHODS: miR-214 and PTEN expression was determined in gastric cancer and matched normal tissues, and human gastric cancer cell lines by quantitative real-time PCR. The roles of miR-214 in cell proliferation, migration and invasion were analyzed with anti-miR-214 transfected cells. In addition, the regulation of PTEN by miR-214 was evaluated by Western blotting and luciferase reporter assays. RESULTS: miR-214 was noted to be highly overexpressed in gastric cancer tissues and cell lines using qRT-PCR. The expression level of miR-214 is significantly associated with clinical progression and poor prognosis according to the analysis of the clinicopathologic data. We also found that the miR-214 levels are inversely correlated with PTEN in tumor tissues. And PTEN expression level is also associated with metastasis and invasion of gastric cancer. In addition, knockdown of miR-214 could significantly inhibit proliferation, migration and invasion of gastric cancer cells. Moreover, we demonstrate that PTEN is regulated negatively by miR-214 through a miR-214 binding site within the 3’-UTR of PTEN at the posttranscriptional level in gastric cancer cells. CONCLUSIONS: These findings indicated that miR-214 regulated the proliferation, migration and invasion by targeting PTEN post-transcriptionally in gastric cancer. It may be a novel potential therapeutic agent for gastric cancer.
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spelling pubmed-37168012013-07-20 MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN Yang, Ting-Song Yang, Xiao-Hu Wang, Xu-Dong Wang, Yi-Ling Zhou, Bo Song, Zhen-Shun Cancer Cell Int Primary Research BACKGROUND: MicroRNAs are a class of small non-coding RNAs that play an important role in various human tumor initiation and progression by regulating gene expression negatively. The aim of this study was to investigate the effect of miR-214 on cell proliferation, migration and invasion, as well as the functional connection between miR-214 and PTEN in gastric cancer. METHODS: miR-214 and PTEN expression was determined in gastric cancer and matched normal tissues, and human gastric cancer cell lines by quantitative real-time PCR. The roles of miR-214 in cell proliferation, migration and invasion were analyzed with anti-miR-214 transfected cells. In addition, the regulation of PTEN by miR-214 was evaluated by Western blotting and luciferase reporter assays. RESULTS: miR-214 was noted to be highly overexpressed in gastric cancer tissues and cell lines using qRT-PCR. The expression level of miR-214 is significantly associated with clinical progression and poor prognosis according to the analysis of the clinicopathologic data. We also found that the miR-214 levels are inversely correlated with PTEN in tumor tissues. And PTEN expression level is also associated with metastasis and invasion of gastric cancer. In addition, knockdown of miR-214 could significantly inhibit proliferation, migration and invasion of gastric cancer cells. Moreover, we demonstrate that PTEN is regulated negatively by miR-214 through a miR-214 binding site within the 3’-UTR of PTEN at the posttranscriptional level in gastric cancer cells. CONCLUSIONS: These findings indicated that miR-214 regulated the proliferation, migration and invasion by targeting PTEN post-transcriptionally in gastric cancer. It may be a novel potential therapeutic agent for gastric cancer. BioMed Central 2013-07-08 /pmc/articles/PMC3716801/ /pubmed/23834902 http://dx.doi.org/10.1186/1475-2867-13-68 Text en Copyright © 2013 Yang et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Primary Research
Yang, Ting-Song
Yang, Xiao-Hu
Wang, Xu-Dong
Wang, Yi-Ling
Zhou, Bo
Song, Zhen-Shun
MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN
title MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN
title_full MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN
title_fullStr MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN
title_full_unstemmed MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN
title_short MiR-214 regulate gastric cancer cell proliferation, migration and invasion by targeting PTEN
title_sort mir-214 regulate gastric cancer cell proliferation, migration and invasion by targeting pten
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3716801/
https://www.ncbi.nlm.nih.gov/pubmed/23834902
http://dx.doi.org/10.1186/1475-2867-13-68
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