Constitutive expression of the Id-1 promoter in human metastatic breast cancer cells is linked with the loss of NF-1/Rb/HDAC-1 transcription repressor complex

Oncogene. 2002 Mar 14;21(12):1812-22. doi: 10.1038/sj.onc.1205252.

Abstract

The helix-loop-helix protein Id-1 is a dominant negative regulator of basic helix-loop-helix transcription factors, and plays a key role in the control of breast epithelial cell growth, invasion and differentiation. Previous investigations in our laboratory have shown that Id-1 mRNA was constitutively expressed in highly aggressive and invasive human breast cancer cells in comparison to non-transformed or non-aggressive cancerous cells, and that this loss of regulation is mediated by a 2.2-kb region of the human Id-1 promoter. Here we show that a 31 bp sequence within this 2.2-kb promoter, located 200 bp upstream of the initiation of transcription, is responsible for the constitutive expression of Id-1 in metastatic human breast cancer cells. Using gel shift experiments, we identified a high molecular weight complex present only in non-aggressive breast cancer cells cultured in serum-free medium and which appear to be necessary for proper Id-1 repression. In contrast, nuclear extracts from highly aggressive and metastatic cell lines do not contain this large molecular weight complex. Using DNA affinity precipitation assays (DAPA), we show that this complex contains SP-1, NF-1, Rb and HDAC-1 proteins. On the basis of these findings, we propose a mechanism for the loss of regulation of Id-1 promoter in invasive and metastatic human breast cancer cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Binding Sites
  • Blotting, Western
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / metabolism
  • DNA Primers / chemistry
  • DNA, Neoplasm / genetics
  • DNA, Neoplasm / metabolism
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Electrophoretic Mobility Shift Assay
  • Epithelial Cells / cytology
  • Epithelial Cells / metabolism
  • Female
  • Gene Deletion
  • Gene Expression Regulation, Neoplastic
  • Helix-Loop-Helix Motifs / genetics
  • Histone Deacetylase 1
  • Histone Deacetylases / genetics*
  • Histone Deacetylases / metabolism
  • Humans
  • Inhibitor of Differentiation Protein 1
  • Mutation / genetics
  • Neoplasm Invasiveness
  • Neurofibromin 1 / genetics*
  • Neurofibromin 1 / metabolism
  • Plasmids
  • Podophyllin / analogs & derivatives*
  • Podophyllin / genetics
  • Podophyllin / metabolism
  • Podophyllotoxin / analogs & derivatives
  • Precipitin Tests
  • Promoter Regions, Genetic / genetics*
  • Repressor Proteins*
  • Retinoblastoma Protein / genetics*
  • Retinoblastoma Protein / metabolism
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism
  • Transfection
  • Tumor Cells, Cultured

Substances

  • DNA Primers
  • DNA, Neoplasm
  • DNA-Binding Proteins
  • ID1 protein, human
  • Inhibitor of Differentiation Protein 1
  • Neurofibromin 1
  • Repressor Proteins
  • Retinoblastoma Protein
  • Transcription Factors
  • mitopodozide
  • Podophyllin
  • HDAC1 protein, human
  • Histone Deacetylase 1
  • Histone Deacetylases
  • Podophyllotoxin