title: MiR-506 Over-Expression Inhibits Proliferation and Metastasis of Breast Cancer Cells.
abstract: BACKGROUND
  This study aimed to investigate the relationship between miR-506 and proliferation and migration of breast cancer cells.
  
  
  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.
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Fei
authors.initials: F
authors.lastname: Yu
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Mingli
authors.initials: M
authors.lastname: Lv
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Dan
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Haidong
authors.initials: H
authors.lastname: Cai
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Lishui
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Qiong
authors.initials: Q
authors.lastname: Luo
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Xueyu
authors.initials: X
authors.lastname: Yuan
authors.affiliation: Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China (mainland).
authors.forename: Zhongwei
authors.initials: Z
authors.lastname: Lv
mesh_terms: D001943:Breast Neoplasms / Q000378:metabolism* / Q000503:physiopathology*; D002452:Cell Count; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000502:physiology; D049109:Cell Proliferation / Q000502:physiology*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D006801:Humans; D066298:In Vitro Techniques; D008055:Lipids; D035683:MicroRNAs / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D018716:Molecular Mimicry / Q000235:genetics; D009362:Neoplasm Metastasis / Q000503:physiopathology*; D014162:Transfection; D014410:Tumor Stem Cell Assay
chemical_list: D008055:Lipids; C086724:Lipofectamine; C561508:MIRN506 microRNA, human; D035683:MicroRNAs