10 June 2015 : Laboratory Research
MiR-506 Over-Expression Inhibits Proliferation and Metastasis of Breast Cancer Cells
Fei YuACE, Mingli LvBCD, Dan LiBCD, Haidong CaiBCD, Lishui MaBCD, Qiong LuoBCD, Xueyu YuanBCD, Zhongwei LvFGDOI: 10.12659/MSM.893522
Med Sci Monit 2015; 21:1687-1692
Abstract
BACKGROUND: This study aimed to investigate the relationship between miR-506 and proliferation and migration of breast cancer cells.
MATERIAL AND METHODS: MiR-506 mimics, inhibitor, and negative control (NC) were transfected into MDA-MB-231 breast cancer cells. Cell proliferation, cell counting, colony formation assay, and Transwell assay were applied to evaluate the proliferation and migration of breast cancer cells. Data are shown as mean ± standard deviation and the experiment was performed 3 times. Statistical analyses were performed with SPSS version 10.0.
RESULTS: At 1 day after transfection, cell proliferation detected by CCK-8 assay was significantly promoted in miR-506 inhibitor when compared with the miR-506 mimics group and the NC group (P<0.05). At 3 days or 5 days after transfection, cell proliferation was markedly inhibited in the miR-506 mimics group, and miR-506 inhibitor was still significantly promoted. Cell counting with a hemocytometer showed similar results to cell proliferation. Colony formation assay showed that the number of colonies in the miR-506 mimics group was significantly smaller than that in the miR-506 inhibitor group and NC group. Transwell assay revealed that the number of migrated cells in miR-506 mimics was markedly smaller than that in the miR-506 inhibitor group and NC group.
CONCLUSIONS: MiR-506 over-expression significantly inhibits the proliferation, colony formation, and migration of breast cancer cells. miR-506 over-expression may thus be able to improve the malignant phenotype of breast cancer cells.
Keywords: Cell Count, Breast Neoplasms - physiopathology, Cell Movement - physiology, Cell Proliferation - physiology, Gene Expression Regulation, Neoplastic - genetics, In Vitro Techniques, Lipids, Molecular Mimicry - genetics, Neoplasm Metastasis - physiopathology, Sincalide, Tumor Stem Cell Assay
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