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The Role of Hypoxia-Induced miR-210 in Cancer Progression
Prolonged hypoxia, the event of insufficient oxygen, is known to upregulate tumor development and growth by promoting the formation of a neoplastic environment. The recent discovery that a subset of cellular microRNAs (miRs) are upregulated during hypoxia, where they function to promote tumor develo...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4394536/ https://www.ncbi.nlm.nih.gov/pubmed/25809609 http://dx.doi.org/10.3390/ijms16036353 |
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author | Dang, Kyvan Myers, Kenneth A. |
author_facet | Dang, Kyvan Myers, Kenneth A. |
author_sort | Dang, Kyvan |
collection | PubMed |
description | Prolonged hypoxia, the event of insufficient oxygen, is known to upregulate tumor development and growth by promoting the formation of a neoplastic environment. The recent discovery that a subset of cellular microRNAs (miRs) are upregulated during hypoxia, where they function to promote tumor development, highlights the importance of hypoxia-induced miRs as targets for continued investigation. miRs are short, non-coding transcripts involved in gene expression and regulation. Under hypoxic conditions, miR-210 becomes highly upregulated in response to hypoxia inducing factors (HIFs). HIF-1α drives miR-210’s overexpression and the resultant alteration of cellular processes, including cell cycle regulation, mitochondria function, apoptosis, angiogenesis and metastasis. Here we discuss hypoxia-induced dysregulation of miR-210 and the resultant changes in miR-210 protein targets that regulate cancer progression. Potential methods of targeting miR-210 as a therapeutic tool are also explored. |
format | Online Article Text |
id | pubmed-4394536 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-43945362015-05-21 The Role of Hypoxia-Induced miR-210 in Cancer Progression Dang, Kyvan Myers, Kenneth A. Int J Mol Sci Review Prolonged hypoxia, the event of insufficient oxygen, is known to upregulate tumor development and growth by promoting the formation of a neoplastic environment. The recent discovery that a subset of cellular microRNAs (miRs) are upregulated during hypoxia, where they function to promote tumor development, highlights the importance of hypoxia-induced miRs as targets for continued investigation. miRs are short, non-coding transcripts involved in gene expression and regulation. Under hypoxic conditions, miR-210 becomes highly upregulated in response to hypoxia inducing factors (HIFs). HIF-1α drives miR-210’s overexpression and the resultant alteration of cellular processes, including cell cycle regulation, mitochondria function, apoptosis, angiogenesis and metastasis. Here we discuss hypoxia-induced dysregulation of miR-210 and the resultant changes in miR-210 protein targets that regulate cancer progression. Potential methods of targeting miR-210 as a therapeutic tool are also explored. MDPI 2015-03-19 /pmc/articles/PMC4394536/ /pubmed/25809609 http://dx.doi.org/10.3390/ijms16036353 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Dang, Kyvan Myers, Kenneth A. The Role of Hypoxia-Induced miR-210 in Cancer Progression |
title | The Role of Hypoxia-Induced miR-210 in Cancer Progression |
title_full | The Role of Hypoxia-Induced miR-210 in Cancer Progression |
title_fullStr | The Role of Hypoxia-Induced miR-210 in Cancer Progression |
title_full_unstemmed | The Role of Hypoxia-Induced miR-210 in Cancer Progression |
title_short | The Role of Hypoxia-Induced miR-210 in Cancer Progression |
title_sort | role of hypoxia-induced mir-210 in cancer progression |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4394536/ https://www.ncbi.nlm.nih.gov/pubmed/25809609 http://dx.doi.org/10.3390/ijms16036353 |
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