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miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1
AIMS: Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide. Many microRNAs (miRNAs), small non-coding RNAs, are involved in regulating cancer cell proliferation, metastasis, migration, invasion and apoptosis. MAIN METHODS: We investigated the expression of miR-135a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4970272/ https://www.ncbi.nlm.nih.gov/pubmed/27486383 http://dx.doi.org/10.1186/s12935-016-0328-z |
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author | Zeng, Yue-Bin Liang, Xing-Hua Zhang, Guang-Xian Jiang, Nan Zhang, Tong Huang, Jian-Ying Zhang, Lei Zeng, Xian-Cheng |
author_facet | Zeng, Yue-Bin Liang, Xing-Hua Zhang, Guang-Xian Jiang, Nan Zhang, Tong Huang, Jian-Ying Zhang, Lei Zeng, Xian-Cheng |
author_sort | Zeng, Yue-Bin |
collection | PubMed |
description | AIMS: Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide. Many microRNAs (miRNAs), small non-coding RNAs, are involved in regulating cancer cell proliferation, metastasis, migration, invasion and apoptosis. MAIN METHODS: We investigated the expression of miR-135a in HCC cell lines and clinical tissues. The effect of miR-135a on migration and invasion of HepG2 and MHCC-97L were examined using wound healing and Transwell assay. We determined the expression of miR-135a, forkhead box O1 (FOXO1), matrix metalloproteinase-2 (MMP-2) and Snail using real-time PCR and western blotting. KEY FINDINGS: We found miR-135a was upregulated in HCC cell lines and tissues. miR-135a overexpression promoted HCC cells migration and invasion, whereas miR-135a inhibition suppressed HCC cells migration and invasion. miR-135a overexpression could upregulate the expression of MMP2, Snail and the phosphorylation of AKT, but decreased FOXO3a phosporylation. Tumor suppressor FOXO1 was the direct target for miR-135a. SIGNIFICANCE: Our results suggested that miR-135a might play an important role in promoting migration and invasion in HCC and presents a novel mechanism of miRNA-mediated direct suppression of FOXO1 in HCC cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12935-016-0328-z) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4970272 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-49702722016-08-03 miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 Zeng, Yue-Bin Liang, Xing-Hua Zhang, Guang-Xian Jiang, Nan Zhang, Tong Huang, Jian-Ying Zhang, Lei Zeng, Xian-Cheng Cancer Cell Int Primary Research AIMS: Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide. Many microRNAs (miRNAs), small non-coding RNAs, are involved in regulating cancer cell proliferation, metastasis, migration, invasion and apoptosis. MAIN METHODS: We investigated the expression of miR-135a in HCC cell lines and clinical tissues. The effect of miR-135a on migration and invasion of HepG2 and MHCC-97L were examined using wound healing and Transwell assay. We determined the expression of miR-135a, forkhead box O1 (FOXO1), matrix metalloproteinase-2 (MMP-2) and Snail using real-time PCR and western blotting. KEY FINDINGS: We found miR-135a was upregulated in HCC cell lines and tissues. miR-135a overexpression promoted HCC cells migration and invasion, whereas miR-135a inhibition suppressed HCC cells migration and invasion. miR-135a overexpression could upregulate the expression of MMP2, Snail and the phosphorylation of AKT, but decreased FOXO3a phosporylation. Tumor suppressor FOXO1 was the direct target for miR-135a. SIGNIFICANCE: Our results suggested that miR-135a might play an important role in promoting migration and invasion in HCC and presents a novel mechanism of miRNA-mediated direct suppression of FOXO1 in HCC cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12935-016-0328-z) contains supplementary material, which is available to authorized users. BioMed Central 2016-08-02 /pmc/articles/PMC4970272/ /pubmed/27486383 http://dx.doi.org/10.1186/s12935-016-0328-z Text en © The Author(s) 2016 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Primary Research Zeng, Yue-Bin Liang, Xing-Hua Zhang, Guang-Xian Jiang, Nan Zhang, Tong Huang, Jian-Ying Zhang, Lei Zeng, Xian-Cheng miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 |
title | miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 |
title_full | miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 |
title_fullStr | miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 |
title_full_unstemmed | miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 |
title_short | miRNA-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box O1 |
title_sort | mirna-135a promotes hepatocellular carcinoma cell migration and invasion by targeting forkhead box o1 |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4970272/ https://www.ncbi.nlm.nih.gov/pubmed/27486383 http://dx.doi.org/10.1186/s12935-016-0328-z |
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