Potentiation of estrogen receptor transcriptional activity by breast cancer amplified sequence 2

Biochem Biophys Res Commun. 2005 Mar 11;328(2):393-8. doi: 10.1016/j.bbrc.2004.12.187.

Abstract

Breast cancer amplified sequence 2 (BCAS2) was initially identified as a gene that was overexpressed and amplified in some breast cancer cell lines. It was later found to be a component of the spliceosome. Here, we identified BCAS2 as an estrogen receptor (ER) alpha interacting protein by yeast two-hybrid screening. In addition to ER alpha, BCAS2 also interacted with ER beta, TR beta, PR, and PPAR gamma in a ligand-independent way. Transient transfection assays revealed that overexpression of BCAS2 enhanced while inhibition of BCAS2 expression attenuated the estrogen receptor-mediated transcription. BCAS2 potentiated the activation function-2 (AF-2) activity of ER alpha but had no effect on the AF-1 activity. This study suggested that BCAS2 might play an important role in breast cancer development by increasing the estrogen receptor's function.

Publication types

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

MeSH terms

  • Animals
  • Breast Neoplasms / metabolism*
  • Cell Line, Tumor
  • Cell Nucleus / metabolism
  • Chlorocebus aethiops
  • Estrogen Receptor alpha / chemistry
  • Estrogen Receptor alpha / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Kidney / metabolism*
  • Neoplasm Proteins / chemistry
  • Neoplasm Proteins / metabolism*
  • Transcriptional Activation*

Substances

  • BCAS2 protein, human
  • Estrogen Receptor alpha
  • Neoplasm Proteins