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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...

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Autores principales: Kong, Ranran, Ma, Yuefeng, Feng, Jie, Li, Shaomin, Zhang, Wei, Jiang, Jiantao, Zhang, Jin, Qiao, Zhe, Yang, Xiaoping, Zhou, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
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.
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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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