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MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma
Background: MicroRNAs (miRNAs) are a class of endogenous, small non-coding RNAs which function as essential posttranscriptional modulators of gene expression tightly involved in a wide range of diseases, including the hepatocellular carcinoma (HCC). Here, the present study was designed to investigat...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Ivyspring International Publisher
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5370505/ https://www.ncbi.nlm.nih.gov/pubmed/28367241 http://dx.doi.org/10.7150/jca.17394 |
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author | Chen, Shu-ying Ma, De-ning Chen, Qiu-dan Zhang, Jing-jun Tian, Yue-ru Wang, Zhi-cheng Cai, Hao Lin, Yong Sun, Hui-chuan |
author_facet | Chen, Shu-ying Ma, De-ning Chen, Qiu-dan Zhang, Jing-jun Tian, Yue-ru Wang, Zhi-cheng Cai, Hao Lin, Yong Sun, Hui-chuan |
author_sort | Chen, Shu-ying |
collection | PubMed |
description | Background: MicroRNAs (miRNAs) are a class of endogenous, small non-coding RNAs which function as essential posttranscriptional modulators of gene expression tightly involved in a wide range of diseases, including the hepatocellular carcinoma (HCC). Here, the present study was designed to investigate the expression levels and cellular roles of miR-200a in HCC. Methods: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-200a in serums and cell lines. Bioinformation analysis, the luciferase reporter assay, qRT-PCR and western blotting were employed to validate Foxa2 as a direct target gene of miR-200a. Cell proliferation, migration and invasion were assessed to identify whether miR-200a could regulate the biological behaviors of HCC cells by targeting Foxa2. Results: In this study, a low level of miR-200a was observed in patients' serums and HCC cell lines. Overexpression of miR-200a in HCC cell lines reduced cell proliferation, migration and invasion. In addition, transcription factor forkhead box A2 (Foxa2) was identified as a novel target of miR-200a and downregulated at mRNA and protein levels in miR-200a overexpressed cells. Meanwhile, restoration of Foxa2 significantly reversed the tumor suppressive effects of miR-200a. Conclusions: These findings indicate that miR-200a regulates the proliferation, migration and invasion of HCC cells by targeting Foxa2, suggesting that miR-200a may function as a potential therapeutic molecular for the diagnosis and treatment of the liver cancer. |
format | Online Article Text |
id | pubmed-5370505 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-53705052017-03-31 MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma Chen, Shu-ying Ma, De-ning Chen, Qiu-dan Zhang, Jing-jun Tian, Yue-ru Wang, Zhi-cheng Cai, Hao Lin, Yong Sun, Hui-chuan J Cancer Research Paper Background: MicroRNAs (miRNAs) are a class of endogenous, small non-coding RNAs which function as essential posttranscriptional modulators of gene expression tightly involved in a wide range of diseases, including the hepatocellular carcinoma (HCC). Here, the present study was designed to investigate the expression levels and cellular roles of miR-200a in HCC. Methods: Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-200a in serums and cell lines. Bioinformation analysis, the luciferase reporter assay, qRT-PCR and western blotting were employed to validate Foxa2 as a direct target gene of miR-200a. Cell proliferation, migration and invasion were assessed to identify whether miR-200a could regulate the biological behaviors of HCC cells by targeting Foxa2. Results: In this study, a low level of miR-200a was observed in patients' serums and HCC cell lines. Overexpression of miR-200a in HCC cell lines reduced cell proliferation, migration and invasion. In addition, transcription factor forkhead box A2 (Foxa2) was identified as a novel target of miR-200a and downregulated at mRNA and protein levels in miR-200a overexpressed cells. Meanwhile, restoration of Foxa2 significantly reversed the tumor suppressive effects of miR-200a. Conclusions: These findings indicate that miR-200a regulates the proliferation, migration and invasion of HCC cells by targeting Foxa2, suggesting that miR-200a may function as a potential therapeutic molecular for the diagnosis and treatment of the liver cancer. Ivyspring International Publisher 2017-02-25 /pmc/articles/PMC5370505/ /pubmed/28367241 http://dx.doi.org/10.7150/jca.17394 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions. |
spellingShingle | Research Paper Chen, Shu-ying Ma, De-ning Chen, Qiu-dan Zhang, Jing-jun Tian, Yue-ru Wang, Zhi-cheng Cai, Hao Lin, Yong Sun, Hui-chuan MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma |
title | MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma |
title_full | MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma |
title_fullStr | MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma |
title_full_unstemmed | MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma |
title_short | MicroRNA-200a inhibits cell growth and metastasis by targeting Foxa2 in hepatocellular carcinoma |
title_sort | microrna-200a inhibits cell growth and metastasis by targeting foxa2 in hepatocellular carcinoma |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5370505/ https://www.ncbi.nlm.nih.gov/pubmed/28367241 http://dx.doi.org/10.7150/jca.17394 |
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