Relation between menin expression and NF-kappaB activity in an intestinal cell line

Mol Cell Endocrinol. 2008 Sep 10;291(1-2):109-15. doi: 10.1016/j.mce.2008.05.019. Epub 2008 Jun 11.

Abstract

In a previous study, we demonstrated that the Men1 gene is mainly expressed in the proliferative crypt compartment of the small intestine and that a reduction of menin expression in the crypt-like IEC-17 cell line induces an increase in proliferation rate concomitant with an increase in cyclin D1 expression. The aim of the present study was to test the hypothesis that the NF-kappaB pathway may be involved in cyclin D1 overexpression. Transcriptional activity of the cyclin D1 gene promoter was increased upon reduction of menin expression. Blockade of the NF-kappaB pathway restored proliferation, cell cycle, cyclin D1 gene transcription and cyclin D1 expression levels to those observed in the presence of menin. These data support a correlation between cyclin D1 expression, NF-kappaB activity and menin expression in this epithelial cell line and are relevant to the physiological function of menin in regulating proliferation in the intestinal epithelium.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Cycle / physiology
  • Cell Line
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism
  • Duodenum / cytology
  • Duodenum / physiology
  • Epithelial Cells / cytology
  • Epithelial Cells / physiology*
  • Gene Expression Regulation
  • Humans
  • Intestinal Mucosa / cytology*
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Rats
  • Transcription Factor RelA / antagonists & inhibitors
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / metabolism*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transcription, Genetic

Substances

  • MEN1 protein, human
  • Men1 protein, rat
  • Proto-Oncogene Proteins
  • Transcription Factor RelA
  • Transcription Factors
  • Cyclin D1