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


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.

DOI: 10.1016/j.bbrc.2013.02.084
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@article{Zhou2013miR206ID, title={miR-206 is down-regulated in breast cancer and inhibits cell proliferation through the up-regulation of cyclinD2.}, author={Jing Zhou and Ye Tian and Juan Li and Binbin Lu and Ming Sun and Yanfen Zou and Rong Kong and Yanhong Luo and Yongguo Shi and Keming Wang and Guozhong Ji}, journal={Biochemical and biophysical research communications}, year={2013}, volume={433 2}, pages={207-12} }