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...

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Main Authors: Kyvan Dang, Kenneth A. Myers
Format: Article
Language:English
Published: MDPI AG 2015-03-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:http://www.mdpi.com/1422-0067/16/3/6353
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spelling doaj-c338a51814084556b99a63800d4233af2020-11-25T01:00:42ZengMDPI AGInternational Journal of Molecular Sciences1422-00672015-03-011636353637210.3390/ijms16036353ijms16036353The Role of Hypoxia-Induced miR-210 in Cancer ProgressionKyvan Dang0Kenneth A. Myers1Department of Biological Sciences, University of the Sciences, 600 S. 43rd Str., Philadelphia, PA 19104, USADepartment of Biological Sciences, University of the Sciences, 600 S. 43rd Str., Philadelphia, PA 19104, USAProlonged 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.http://www.mdpi.com/1422-0067/16/3/6353miR-210hypoxiamicroRNAapoptosisangiogenesiscancer
collection DOAJ
language English
format Article
sources DOAJ
author Kyvan Dang
Kenneth A. Myers
spellingShingle Kyvan Dang
Kenneth A. Myers
The Role of Hypoxia-Induced miR-210 in Cancer Progression
International Journal of Molecular Sciences
miR-210
hypoxia
microRNA
apoptosis
angiogenesis
cancer
author_facet Kyvan Dang
Kenneth A. Myers
author_sort Kyvan Dang
title The Role of Hypoxia-Induced miR-210 in Cancer Progression
title_short 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_sort role of hypoxia-induced mir-210 in cancer progression
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2015-03-01
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.
topic miR-210
hypoxia
microRNA
apoptosis
angiogenesis
cancer
url http://www.mdpi.com/1422-0067/16/3/6353
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