Inhibition of PKR Activity is Required for Survival of Breast Cancer

Abstract

PKR is an interferon-inducible protein kinase, which has recently been discovered to have pleiotropic effects on the growth and differentiation of normal and neoplastic cells. We reported a direct correlation between PKR expression and differentiation in a variety of human tumors and in normal squamous epithelial, and an inverse association between%PKR expression and proliferation in head and neck cancer. The mechanisms by which PKR produced such effects are being intensively studied. Phosphorylation of its major substrate, eIF-2alpha, leads to a selective inhibition of protein synthesis. PKR also phosphorylates IkB, freeing NFkB to tranlocate to the nucleus and induce transcription of a number of gene products. PKR-induced apoptosis has recently been reported to be co-dependent on both the eIF2alpha and NFKB pathways in HeLa cells. Breast cancer was utilized as a model system to determine the role of PKR in loss of hormone and growth factor dependence in human cancers, as it appears inactive or hypoactive, as determined by eIF-2alpha phosphyorylation in this system. We hypothesized that hormone deprivation induces apoptosis in dependent cell lines through a PKR: NFKB mediated process, but this pathway is abrogated in hormone-independent cell lines.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Jan 01, 2003
Accession Number
ADA426882

Entities

People

  • George K. Haines

Organizations

  • Northwestern University

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cells
  • Chemical Compounds
  • Chemistry
  • Deprivation
  • Fibroblasts
  • Growth Factors
  • Hormones
  • Inhibition
  • Interferon
  • Neoplasms
  • Phosphorylation
  • Proteins
  • Substrates

Fields of Study

  • Medicine

Readers

  • Breast cancer cell signaling and growth regulation.
  • Molecular Biology and Genetics