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The role of miR-210 in Prostate Cancer tumour development

McElhatton, Niall, Walsh, Colum and McKenna, Declan (2016) The role of miR-210 in Prostate Cancer tumour development. Ulster Medical Journal, 87 (1). p. 13. [Journal article]

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Abstract

Background: Hypoxia in prostate tumours has been linked with promotion of disease progression and metastasis. miR-210 is a microRNA which is apparently affected by hypoxia, but this relationship has not been extensively studied in a prostate cancer setting. Therefore, in this study, we investigate the link between hypoxia and miR-210 in prostate cancer cells.Methods: We have used 2D and 3D cell prostate cell models of hypoxia to investigate the functionality of miR-210. Expression levels of miR-210 have been measured by qPCR and functional bioassays used to examine its effect on prostate cell behaviour. Target genes have been identified and bioinformatic analysis has been employed to investigate a clinical significance for miR-210 in prostate cancer.Results: miR-210 is induced by hypoxia in prostate cancer cell-lines. Over-expression of miR-210 impacts upon target genes, including SP1 and TPD52, which in turns affects cell proliferation. Data-mining of online repositories of clinical data and bioinformatic analysis of miR-210 cellular networks reveal that miR-210 plays a key role in a number of important cell processes, the dysregulation of which can lead to development of prostate cancer.Conclusions: We propose that miR-210 could be an important microRNA in the pathogenesis of prostate cancer and has potential as a biomarker in this disease.

Item Type:Journal article
Keywords:microRNA, miR-210, Prostate cancer, hypoxia
Faculties and Schools:Faculty of Life and Health Sciences > School of Biomedical Sciences
Faculty of Life and Health Sciences
Research Institutes and Groups:Biomedical Sciences Research Institute > Genomic Medicine
Biomedical Sciences Research Institute
ID Code:36078
Deposited By: Dr Declan McKenna
Deposited On:12 Oct 2016 08:26
Last Modified:17 Oct 2017 16:26

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