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The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A
BACKGROUND: miR-126 is a key regulator of oncogenic processes. It is functionally linked to cellular proliferation, survival and migration. Vascular endothelial growth factor A (VEGF-A), which is regarded as a tumorgenesis activator, could directly target miR-126 in several tumors. However, the mech...
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/PMC5415818/ https://www.ncbi.nlm.nih.gov/pubmed/28536606 http://dx.doi.org/10.1186/s11658-016-0004-2 |
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author | Kong, Ranran Ma, Yuefeng Feng, Jie Li, Shaomin Zhang, Wei Jiang, Jiantao Zhang, Jin Qiao, Zhe Yang, Xiaoping Zhou, Bin |
author_facet | Kong, Ranran Ma, Yuefeng Feng, Jie Li, Shaomin Zhang, Wei Jiang, Jiantao Zhang, Jin Qiao, Zhe Yang, Xiaoping Zhou, Bin |
author_sort | Kong, Ranran |
collection | PubMed |
description | BACKGROUND: miR-126 is a key regulator of oncogenic processes. It is functionally linked to cellular proliferation, survival and migration. Vascular endothelial growth factor A (VEGF-A), which is regarded as a tumorgenesis activator, could directly target miR-126 in several tumors. However, the mechanism in esophageal cancer remains unclear. METHODS AND RESULTS: In this study, the expression of miR-126 and VEGF-A were assessed in esophageal cancer tissues and esophageal cancer cell lines. We found that miR-126 has significantly lower expression in esophageal cancer tissues and esophageal cancer cell lines than in healthy tissues, while the expression of VEGF-A is high. Luciferase reporter assays were performed to investigate the relationship between VEGF-A and miR-126. We confirmed that VEGF-A is a target for miR-126. Furthermore, the proliferation of esophageal cancer cells with miR-126 overexpression and miR-126 knockdown was monitored using the MTT assay. The results showed that miR-126 could inhibit esophageal cancer cell proliferation in vitro. The effect of miR-126 was also detected in BALB/c nude mice with transplanted esophageal cancer cells. In vivo study showed that tumor growth was significantly suppressed by miR-126 overexpression. CONCLUSIONS: We believe that restoring miR-126 levels may be a promising therapeutic approach in cases of esophageal cancer. |
format | Online Article Text |
id | pubmed-5415818 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-54158182017-05-23 The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A Kong, Ranran Ma, Yuefeng Feng, Jie Li, Shaomin Zhang, Wei Jiang, Jiantao Zhang, Jin Qiao, Zhe Yang, Xiaoping Zhou, Bin Cell Mol Biol Lett Short Communication BACKGROUND: miR-126 is a key regulator of oncogenic processes. It is functionally linked to cellular proliferation, survival and migration. Vascular endothelial growth factor A (VEGF-A), which is regarded as a tumorgenesis activator, could directly target miR-126 in several tumors. However, the mechanism in esophageal cancer remains unclear. METHODS AND RESULTS: In this study, the expression of miR-126 and VEGF-A were assessed in esophageal cancer tissues and esophageal cancer cell lines. We found that miR-126 has significantly lower expression in esophageal cancer tissues and esophageal cancer cell lines than in healthy tissues, while the expression of VEGF-A is high. Luciferase reporter assays were performed to investigate the relationship between VEGF-A and miR-126. We confirmed that VEGF-A is a target for miR-126. Furthermore, the proliferation of esophageal cancer cells with miR-126 overexpression and miR-126 knockdown was monitored using the MTT assay. The results showed that miR-126 could inhibit esophageal cancer cell proliferation in vitro. The effect of miR-126 was also detected in BALB/c nude mice with transplanted esophageal cancer cells. In vivo study showed that tumor growth was significantly suppressed by miR-126 overexpression. CONCLUSIONS: We believe that restoring miR-126 levels may be a promising therapeutic approach in cases of esophageal cancer. BioMed Central 2016-07-28 /pmc/articles/PMC5415818/ /pubmed/28536606 http://dx.doi.org/10.1186/s11658-016-0004-2 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 | Short Communication Kong, Ranran Ma, Yuefeng Feng, Jie Li, Shaomin Zhang, Wei Jiang, Jiantao Zhang, Jin Qiao, Zhe Yang, Xiaoping Zhou, Bin The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A |
title | The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A |
title_full | The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A |
title_fullStr | The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A |
title_full_unstemmed | The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A |
title_short | The crucial role of miR-126 on suppressing progression of esophageal cancer by targeting VEGF-A |
title_sort | crucial role of mir-126 on suppressing progression of esophageal cancer by targeting vegf-a |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5415818/ https://www.ncbi.nlm.nih.gov/pubmed/28536606 http://dx.doi.org/10.1186/s11658-016-0004-2 |
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