miR-100 suppresses IGF2 and inhibits breast tumorigenesis by interfering with proliferation and survival signaling

Oncogene. 2013 Jul 4;32(27):3306-10. doi: 10.1038/onc.2012.372. Epub 2012 Aug 27.


Dysregulation of micro RNAs is crucially implicated in tumorigenesis. We detected downregulation of miR-100 in breast cancer cells, leading to an upregulation of the proliferation- and survival-promoting oncogene insulin-like growth factor (IGF) 2. Stable overexpression of miR-100 strongly reduced IGF2 expression and inhibited tumor growth. In invasive human breast tumors, miR-100 was reduced about fourfold as compared with benign patient samples, whereas IGF2 was strongly enhanced. MiR-100 has also been shown to suppress other proteins of the IGF/mammalian target of rapamycin (mTOR) signaling cascade in different human tumors. Our results reveal miR-100 as a context-dependent master regulator of the IGF/mTOR pathway and a potential target for therapeutic approaches.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Blotting, Western
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Proliferation*
  • Cell Survival / physiology
  • Cell Transformation, Neoplastic / genetics*
  • Cell Transformation, Neoplastic / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • Insulin-Like Growth Factor II / genetics
  • Insulin-Like Growth Factor II / metabolism*
  • Mice
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Mutagenesis, Site-Directed
  • Polymerase Chain Reaction
  • Signal Transduction / physiology*
  • TOR Serine-Threonine Kinases / metabolism


  • IGF2 protein, human
  • MIRN100 microRNA, human
  • MicroRNAs
  • Insulin-Like Growth Factor II
  • MTOR protein, human
  • TOR Serine-Threonine Kinases