Induction of cell-free, in vitro transcription by recombinant androgen receptor peptides

J Steroid Biochem Mol Biol. 1996 Nov;59(3-4):243-50. doi: 10.1016/s0960-0760(96)00116-1.

Abstract

An in vitro, cell-free transcription system, based on prostate-derived transcriptional machinery and very powerful androgen response elements (AREs), has been developed. Multiple (p(ARR3)LovTATA) AREs from the androgen-regulated probasin gene were linked to G-free cassettes and used in nuclear extracts prepared from prostate carcinoma cell lines (PC3 and LNCaP cells) to test specific induction of transcription by full-length AR and by glutathione-S-transferase (GST)-fusion peptides in which the androgen receptor (AR) DNA-binding domain alone (AR524-649), or together with the ligand-binding domain (AR524-902), or a portion of the NH2-terminal domain (AR232-649) were incorporated. In the presence of AR, nuclear extracts from PC3 cells had greater activity in supporting transcription than those from LNCaP cells; and lower background activity than those from HeLa cells. All of the AR forms correctly initiated in vitro transcription of ARE-templates in an androgen-independent manner. The amount of specific, inducible transcript was dependent on the concentration of AR peptide present. AR524-902 was the most potent transactivator tested, with the maximal level of specific transcript over 900-fold higher than the minimal level. At all concentrations this peptide was three to four times more active than either AR524-649 or AR232-649. In conclusion, we have developed a very specific and sensitive cell-free transcription system for delineating trans-activational regions of the AR.

Publication types

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

MeSH terms

  • Androgen-Binding Protein / genetics
  • Animals
  • Carcinoma
  • Cell Extracts
  • Cell Nucleus
  • Cell-Free System
  • Escherichia coli / genetics
  • Glutathione Transferase / genetics
  • HeLa Cells
  • Humans
  • Male
  • Peptides
  • Prostatic Neoplasms
  • Rats
  • Receptors, Androgen / genetics*
  • Recombinant Fusion Proteins
  • Sensitivity and Specificity
  • Transcription, Genetic*
  • Transcriptional Activation
  • Tumor Cells, Cultured

Substances

  • Androgen-Binding Protein
  • Cell Extracts
  • Peptides
  • Receptors, Androgen
  • Recombinant Fusion Proteins
  • probasin
  • Glutathione Transferase