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The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene
BACKGROUND: MiRNAs was recognized as vital regulators involved in cancer development. Radioresistance remains a major obstacle for effective treatment of cancers. The mechanisms on the miRNA-mediated radioresistance of cancers are still poorly understood. The main subject of this study is to find ne...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6240238/ https://www.ncbi.nlm.nih.gov/pubmed/30479565 http://dx.doi.org/10.1186/s12935-018-0689-6 |
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author | Zang, Chunbao Zhao, Fangfang Hua, Lei Pu, Youguang |
author_facet | Zang, Chunbao Zhao, Fangfang Hua, Lei Pu, Youguang |
author_sort | Zang, Chunbao |
collection | PubMed |
description | BACKGROUND: MiRNAs was recognized as vital regulators involved in cancer development. Radioresistance remains a major obstacle for effective treatment of cancers. The mechanisms on the miRNA-mediated radioresistance of cancers are still poorly understood. The main subject of this study is to find new miRNA biomarker that regulates the radioresistance of esophageal cancer (EC). METHODS: The cumulative dose of radiation assays were used to screen the EC radioresistant cell lines. Wound-healing and invasion assays were used to characterize the properties of these cell lines. The following survival fraction experiments were performed to test the effects of miR-199a-3p and AK4 in the radioresistance of EC. In addition, we used the luciferase reporter assays to identify the putative underlying mechanism that relates to the miR-199a-3p regulated radio-resistance. RESULTS: We found that the AK4 gene is one of the targets of miR-199a-3p, which promotes the radioresistance of EC cells. The following experiments by force reversal of the miR-199a-3p or AK4 levels confirmed the relationship of miR-199a-3p and AK4 with the radioresistance of EC cells. In addition, the activities of several signaling pathway were drastically altered by the forced changes of the miR-199a-3p level in EC cells. CONCLUSION: Taken together, we found that miR-199a-3p can be potentially used as a biomarker for the EC radioresistance. Moreover, these results provides new insights into the mechanism on the radioresistance of EC cells, and also might guide the clinical therapy of EC. |
format | Online Article Text |
id | pubmed-6240238 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-62402382018-11-26 The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene Zang, Chunbao Zhao, Fangfang Hua, Lei Pu, Youguang Cancer Cell Int Primary Research BACKGROUND: MiRNAs was recognized as vital regulators involved in cancer development. Radioresistance remains a major obstacle for effective treatment of cancers. The mechanisms on the miRNA-mediated radioresistance of cancers are still poorly understood. The main subject of this study is to find new miRNA biomarker that regulates the radioresistance of esophageal cancer (EC). METHODS: The cumulative dose of radiation assays were used to screen the EC radioresistant cell lines. Wound-healing and invasion assays were used to characterize the properties of these cell lines. The following survival fraction experiments were performed to test the effects of miR-199a-3p and AK4 in the radioresistance of EC. In addition, we used the luciferase reporter assays to identify the putative underlying mechanism that relates to the miR-199a-3p regulated radio-resistance. RESULTS: We found that the AK4 gene is one of the targets of miR-199a-3p, which promotes the radioresistance of EC cells. The following experiments by force reversal of the miR-199a-3p or AK4 levels confirmed the relationship of miR-199a-3p and AK4 with the radioresistance of EC cells. In addition, the activities of several signaling pathway were drastically altered by the forced changes of the miR-199a-3p level in EC cells. CONCLUSION: Taken together, we found that miR-199a-3p can be potentially used as a biomarker for the EC radioresistance. Moreover, these results provides new insights into the mechanism on the radioresistance of EC cells, and also might guide the clinical therapy of EC. BioMed Central 2018-11-16 /pmc/articles/PMC6240238/ /pubmed/30479565 http://dx.doi.org/10.1186/s12935-018-0689-6 Text en © The Author(s) 2018 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 Zang, Chunbao Zhao, Fangfang Hua, Lei Pu, Youguang The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene |
title | The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene |
title_full | The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene |
title_fullStr | The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene |
title_full_unstemmed | The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene |
title_short | The miR-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the AK4 gene |
title_sort | mir-199a-3p regulates the radioresistance of esophageal cancer cells via targeting the ak4 gene |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6240238/ https://www.ncbi.nlm.nih.gov/pubmed/30479565 http://dx.doi.org/10.1186/s12935-018-0689-6 |
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