Par-4 drives trafficking and activation of Fas and Fasl to induce prostate cancer cell apoptosis and tumor regression

Cancer Res. 2001 Oct 1;61(19):7255-63.

Abstract

Prostate cancer cells are generally resistant to apoptosis by conventional therapy. During a search for molecules that may overcome prostate cancer cell survival mechanisms, we identified the prostate apoptosis response-4 (Par-4) gene. Par-4 induced apoptosis of selective prostate cancer cells PC-3, DU-145, and TSU-Pr and caused tumor regression by inhibition of NF-kappaB activity and cell membrane trafficking of Fas and FasL that leads to the activation of the Fas-Fas-associated death domain-caspase-8 pro-death pathway. Neither Fas pathway activation alone nor inhibition of NF-kappaB activity with IkappaB-super repressor was sufficient to induce apoptosis of prostate cancer cells. Coregulation of these two pathways was essential and sufficient for Par-4 to induce apoptosis. On the other hand, prostate cancer cells LNCaP or normal prostatic epithelial cells that were resistant to apoptosis by Par-4 did not show Fas or FasL trafficking. These findings identify a mechanism of apoptosis by Par-4 and suggest that Par-4 may have therapeutic potential.

Publication types

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

MeSH terms

  • Androgens / physiology
  • Animals
  • Apoptosis / genetics
  • Apoptosis / physiology*
  • Apoptosis Regulatory Proteins
  • Carrier Proteins / antagonists & inhibitors
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology*
  • Cell Membrane / metabolism
  • Fas Ligand Protein
  • Humans
  • Intracellular Signaling Peptides and Proteins*
  • Male
  • Membrane Glycoproteins / metabolism
  • Membrane Glycoproteins / physiology*
  • Mice
  • NF-kappa B / antagonists & inhibitors
  • NF-kappa B / physiology
  • Neoplasms, Hormone-Dependent / genetics
  • Neoplasms, Hormone-Dependent / pathology
  • PTEN Phosphohydrolase
  • Phosphoric Monoester Hydrolases / antagonists & inhibitors
  • Phosphoric Monoester Hydrolases / genetics
  • Phosphoric Monoester Hydrolases / physiology
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / pathology*
  • Prostatic Neoplasms / therapy
  • Proto-Oncogene Proteins c-bcl-2 / physiology
  • Signal Transduction / physiology
  • Transcription, Genetic / physiology
  • Transfection
  • Tumor Suppressor Protein p53 / physiology
  • Tumor Suppressor Proteins*
  • Xenograft Model Antitumor Assays
  • bcl-X Protein
  • fas Receptor / metabolism
  • fas Receptor / physiology*

Substances

  • Androgens
  • Apoptosis Regulatory Proteins
  • BCL2L1 protein, human
  • Bcl2l1 protein, mouse
  • Carrier Proteins
  • FASLG protein, human
  • Fas Ligand Protein
  • Fasl protein, mouse
  • Intracellular Signaling Peptides and Proteins
  • Membrane Glycoproteins
  • NF-kappa B
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • bcl-X Protein
  • fas Receptor
  • prostate apoptosis response-4 protein
  • Phosphoric Monoester Hydrolases
  • PTEN Phosphohydrolase
  • PTEN protein, human