Mir-17-5p regulates breast cancer cell proliferation by inhibiting translation of AIB1 mRNA

Mol Cell Biol. 2006 Nov;26(21):8191-201. doi: 10.1128/MCB.00242-06. Epub 2006 Aug 28.

Abstract

MicroRNAs are an extensive family of approximately 22-nucleotide-long noncoding RNAs expressed in a wide range of eukaryotes, including humans, and they are important in development and disease. We found that microRNA Mir-17-5p has extensive complementarity to the mRNA of AIB1 (named for "amplified in breast cancer 1"). Cell culture experiments showed that AIB1 expression was downregulated by Mir-17-5p, primarily through translational inhibition. Expression of Mir-17-5p was low in breast cancer cell lines. We also found that downregulation of AIB1 by Mir-17-5p resulted in decreased estrogen receptor-mediated, as well as estrogen receptor-independent, gene expression and decreased proliferation of breast cancer cells. Mir-17-5p also completely abrogated the insulin-like growth factor 1-mediated, anchorage-independent growth of breast cancer cells. Our results reveal that Mir-17-5p has a role as a tumor suppressor in breast cancer cells.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Breast Neoplasms* / genetics
  • Breast Neoplasms* / metabolism
  • Breast Neoplasms* / pathology
  • Cell Line, Tumor
  • Cell Proliferation*
  • E2F1 Transcription Factor / genetics
  • E2F1 Transcription Factor / metabolism
  • Estrogens / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Histone Acetyltransferases / genetics
  • Histone Acetyltransferases / metabolism*
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Nuclear Receptor Coactivator 3
  • Protein Biosynthesis*
  • Receptors, Estrogen / genetics
  • Receptors, Estrogen / metabolism
  • Signal Transduction / physiology
  • Trans-Activators / genetics
  • Trans-Activators / metabolism*

Substances

  • E2F1 Transcription Factor
  • E2F1 protein, human
  • Estrogens
  • MicroRNAs
  • Receptors, Estrogen
  • Trans-Activators
  • Histone Acetyltransferases
  • NCOA3 protein, human
  • Nuclear Receptor Coactivator 3