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Biochem Biophys Res Commun. 2013 Apr 5;433(2):207-12. doi: 10.1016/j.bbrc.2013.02.084. Epub 2013 Mar 1.

miR-206 is down-regulated in breast cancer and inhibits cell proliferation through the up-regulation of cyclinD2.

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  • 1Department of Oncology, Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, PR China. zhougjing9888@163.com

Abstract

MicroRNAs act as important gene regulators in human genomes, and their aberrant expression is linked to many malignancies. Aberrant expression of miR-206 has been frequently reported in cancer studies; however, the role and mechanism of its function in breast cancer remains unclear. Quantitative real-time PCR was performed to detect the relative expression levels of miR-206 in breast cancer and normal breast tissues. Lower expression of miR-206 in breast cancer tissues was associated with larger tumour size and a more advanced clinical stage. Further in vitro observations showed that the enforced expression of miR-206 in MCF-7 breast cancer cells inhibited cell growth by blocking the G1/S transition and suppressed cell proliferation and colony formation, implying that miR-206 functions as a tumour suppressor in the progression of breast cancer. Interestingly, Luciferase assays first revealed that miR-206 inhibited cyclinD2 expression by targeting two binding sites in the 3'-untranslated region of cyclinD2 mRNA. qRT-PCR and Western blot assays verified that miR-206 reduced cyclinD2 expression at both the mRNA and protein levels. A reverse correlation between miR-206 and cyclinD2 expression was noted in breast cancer tissues. Altogether, our results identify a crucial tumour suppressive role of miR-206 in the progression of breast cancer, at least partly via up-regulation of the expression of cyclinD2, and suggest that miR-206 might be a candidate prognostic predictor or an anticancer therapeutic target for breast cancer patients.

Copyright © 2013 Elsevier Inc. All rights reserved.

PMID:
23466356
[PubMed - indexed for MEDLINE]
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