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      Multiple functions of hypoxia-regulated miR-210 in cancer

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          Abstract

          MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression post-transcriptionally. miRNAs can be induced by a variety of stresses such as hypoxia, and are involved in diverse biological processes including differentiation, cell proliferation, cell death, and tumorigenesis. Hypoxia, a common feature of tumor microenvironment, can induce a number of miRNAs expression. miRNA-210 (miR-210) is one of the hypoxia-regulated-miRNAs, which has been investigated extensively in cancer. However, paradoxically opposing results were documented regarding whether it is an oncogene or a tumor suppressor, and whether it is a positive or negative prognostic biomarker. In the present review, we focus on the following investigations of miR-210: 1) its functions of as an oncogene, 2) its functions as a tumor suppressor, 3) its functions in mitochondrial metabolism, and finally, the diagnostic and prognostic value of miR-210 in cancer researches.

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          Hypoxia in cancer: significance and impact on clinical outcome.

          Peter Vaupel, Arnulf Mayer (2007)
          Hypoxia, a characteristic feature of locally advanced solid tumors, has emerged as a pivotal factor of the tumor (patho-)physiome since it can promote tumor progression and resistance to therapy. Hypoxia represents a "Janus face" in tumor biology because (a) it is associated with restrained proliferation, differentiation, necrosis or apoptosis, and (b) it can also lead to the development of an aggressive phenotype. Independent of standard prognostic factors, such as tumor stage and nodal status, hypoxia has been suggested as an adverse prognostic factor for patient outcome. Studies of tumor hypoxia involving the direct assessment of the oxygenation status have suggested worse disease-free survival for patients with hypoxic cervical cancers or soft tissue sarcomas. In head & neck cancers the studies suggest that hypoxia is prognostic for survival and local control. Technical limitations of the direct O(2) sensing technique have prompted the use of surrogate markers for tumor hypoxia, such as hypoxia-related endogenous proteins (e.g., HIF-1alpha, GLUT-1, CA IX) or exogenous bioreductive drugs. In many - albeit not in all - studies endogenous markers showed prognostic significance for patient outcome. The prognostic relevance of exogenous markers, however, appears to be limited. Noninvasive assessment of hypoxia using imaging techniques can be achieved with PET or SPECT detection of radiolabeled tracers or with MRI techniques (e.g., BOLD). Clinical experience with these methods regarding patient prognosis is so far only limited. In the clinical studies performed up until now, the lack of standardized treatment protocols, inconsistencies of the endpoints characterizing the oxygenation status and methodological differences (e.g., different immunohistochemical staining procedures) may compromise the power of the prognostic parameter used.
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            A microRNA signature of hypoxia.

            Ritu Kulshreshtha, Manuela Ferracin, Sylwia E. Wojcik … (2007)
            Recent research has identified critical roles for microRNAs in a large number of cellular processes, including tumorigenic transformation. While significant progress has been made towards understanding the mechanisms of gene regulation by microRNAs, much less is known about factors affecting the expression of these noncoding transcripts. Here, we demonstrate for the first time a functional link between hypoxia, a well-documented tumor microenvironment factor, and microRNA expression. Microarray-based expression profiles revealed that a specific spectrum of microRNAs (including miR-23, -24, -26, -27, -103, -107, -181, -210, and -213) is induced in response to low oxygen, at least some via a hypoxia-inducible-factor-dependent mechanism. Select members of this group (miR-26, -107, and -210) decrease proapoptotic signaling in a hypoxic environment, suggesting an impact of these transcripts on tumor formation. Interestingly, the vast majority of hypoxia-induced microRNAs are also overexpressed in a variety of human tumors.
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              MicroRNA-210 modulates endothelial cell response to hypoxia and inhibits the receptor tyrosine kinase ligand Ephrin-A3.

              Pasquale Fasanaro, Yuri D'Alessandra, Valeria Di Stefano … (2008)
              MicroRNAs (miRNAs) are small non-protein-coding RNAs that function as negative gene expression regulators. In the present study, we investigated miRNAs role in endothelial cell response to hypoxia. We found that the expression of miR-210 progressively increased upon exposure to hypoxia. miR-210 overexpression in normoxic endothelial cells stimulated the formation of capillary-like structures on Matrigel and vascular endothelial growth factor-driven cell migration. Conversely, miR-210 blockade via anti-miRNA transfection inhibited the formation of capillary-like structures stimulated by hypoxia and decreased cell migration in response to vascular endothelial growth factor. miR-210 overexpression did not affect endothelial cell growth in both normoxia and hypoxia. However, anti-miR-210 transfection inhibited cell growth and induced apoptosis, in both normoxia and hypoxia. We determined that one relevant target of miR-210 in hypoxia was Ephrin-A3 since miR-210 was necessary and sufficient to down-modulate its expression. Moreover, luciferase reporter assays showed that Ephrin-A3 was a direct target of miR-210. Ephrin-A3 modulation by miR-210 had significant functional consequences; indeed, the expression of an Ephrin-A3 allele that is not targeted by miR-210 prevented miR-210-mediated stimulation of both tubulogenesis and chemotaxis. We conclude that miR-210 up-regulation is a crucial element of endothelial cell response to hypoxia, affecting cell survival, migration, and differentiation.
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                Author and article information

                Contributors
                Qin Qin
                Wei Furong
                Li Baosheng
                Journal
                Journal ID (nlm-ta): J Exp Clin Cancer Res
                Journal ID (iso-abbrev): J. Exp. Clin. Cancer Res
                Title: Journal of Experimental & Clinical Cancer Research : CR
                Publisher: BioMed Central
                ISSN (Print): 0392-9078
                ISSN (Electronic): 1756-9966
                Publication date Collection: 2014
                Publication date (Electronic): 9 June 2014
                Volume: 33
                Issue: 1
                Page: 50
                Affiliations
                [1 ]Department of Radiation Oncology, Shandong Cancer Hospital, Shandong University, Jiyan Road 440, Jinan 250117, P.R. China
                [2 ]Department of Radiation Oncology, Shandong Cancer Hospital, Shandong Academy of Medical Sciences, Jinan 250117, P.R. China
                [3 ]Institute of Basic Medicine, Shandong Academy of Medical Sciences, Jingshi Road 18877, Jinan 250062, P.R. China
                Article
                Publisher ID: 1756-9966-33-50
                DOI: 10.1186/1756-9966-33-50
                PMC ID: 4060094
                PubMed ID: 24909053
                SO-VID: 855e20b7-35e0-417b-afa7-22991e919e6e
                Copyright © Copyright © 2014 Qin et al.; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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.

                History
                Date received : 11 May 2014
                Date accepted : 1 June 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: microrna,hypoxia,mir-210,proliferation,apoptosis,angiogenesis,metabolism,diagnosis,prognosis
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: microrna, hypoxia, mir-210, proliferation, apoptosis, angiogenesis, metabolism, diagnosis, prognosis

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