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Inhibition of Cell Proliferation and Migration by miR-509-3p That Targets CDK2, Rac1, and PIK3C2A

  • Yoon, Sena (Graduate School of Biotechnology, Kyung Hee University) ;
  • Han, Eunji (Graduate School of Biotechnology, Kyung Hee University) ;
  • Choi, Young-Chul (Graduate School of Biotechnology, Kyung Hee University) ;
  • Kee, Honghwan (Graduate School of Biotechnology, Kyung Hee University) ;
  • Jeong, Yongsu (Graduate School of Biotechnology, Kyung Hee University) ;
  • Yoon, Jaeseung (Graduate School of Biotechnology, Kyung Hee University) ;
  • Baek, Kwanghee (Graduate School of Biotechnology, Kyung Hee University)
  • Received : 2013.12.02
  • Accepted : 2014.03.11
  • Published : 2014.04.30

Abstract

CDK2 is a key regulator of cell cycle progression. In this study, we screened for miRNAs targeting CDK2 using a luciferase-3'-untranslated region reporter assay. Among 11 hit miRNAs, miR-509-3p reduced CDK2 protein levels and significantly inhibited cancer cell growth. Microarray, Western blotting, and luciferase reporter analyses revealed additional targets of miR-509-3p, including Rac1 and PIK3C2A. Overexpression of miR-509-3p induced G1 cell-cycle arrest and inhibited colony formation and migration. RNAi experiments indicated that the growth-inhibitory effects of miR-509-3p may occur through down-regulation of CDK2, Rac1, and PIK3C2A. Targeting of multiple growth regulatory genes by miR-509-3p may contribute to effective anti-cancer therapy.

Keywords

References

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