Expression of RAC 3, a steroid hormone receptor co-activator in prostate cancer

Br J Cancer. 2001 Dec 14;85(12):1928-36. doi: 10.1054/bjoc.2001.2179.

Abstract

RAC 3, one of the p160 family of co-activators is known to enhance the transcriptional activity of a number of steroid receptors. As co-activators are also known to enhance androgen receptor (AR) activity, we investigated the role of RAC 3 in the context of prostate cancer. In prostate cancer cell lines, we found variable levels of the RAC 3 protein with highest expression seen in AR-positive LNCaP cells, moderate expression in AR-negative PC 3 cells and low-level expression in AR-negative DU 145 cells. Immuno-precipitation studies showed that endogenous RAC 3 interacted with the AR in vivo and transfection assays confirmed that RAC 3 enhanced AR transcriptional activity. In clinical prostate tissue, we found strong RAC 3 mRNA expression and immuno-histochemistry demonstrated that in benign tissue, the protein was expressed predominantly in luminal cells, while in primary malignant epithelium it was more homogeneously expressed. In a series of 37 patients, the levels of RAC 3 expression correlated significantly with tumour grade (P = 0.01) and stage of disease (P = 0.03) but not with serum PSA levels. In addition moderate or high RAC 3 expression was associated with poorer disease-specific survival (P = 0.03). We conclude that RAC 3 is an important co-activator of the AR in the prostate and may have an important role in the progression of prostate cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism*
  • Aged
  • Aged, 80 and over
  • Androgens*
  • Biomarkers, Tumor / blood
  • Disease Progression
  • Epithelial Cells / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • In Situ Hybridization
  • Male
  • Middle Aged
  • Neoplasm Proteins / biosynthesis*
  • Neoplasm Proteins / genetics
  • Neoplasm Staging
  • Neoplasms, Hormone-Dependent / genetics
  • Neoplasms, Hormone-Dependent / metabolism*
  • Neoplasms, Hormone-Dependent / pathology
  • Nuclear Receptor Coactivator 3
  • Prostate-Specific Antigen / blood
  • Prostatic Hyperplasia / metabolism
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • RNA, Neoplasm / biosynthesis
  • RNA, Neoplasm / genetics
  • Receptors, Androgen / metabolism
  • Trans-Activators / biosynthesis*
  • Trans-Activators / genetics
  • Transcription Factors*
  • Transcription, Genetic
  • Transfection
  • Tumor Cells, Cultured / metabolism

Substances

  • Androgens
  • Biomarkers, Tumor
  • Neoplasm Proteins
  • RNA, Messenger
  • RNA, Neoplasm
  • Receptors, Androgen
  • Trans-Activators
  • Transcription Factors
  • Nuclear Receptor Coactivator 3
  • Prostate-Specific Antigen