Fatty Acid Synthesis and Control of Caspase 2 in Prostate Cancer

Abstract

Although prostate cancers are initially responsive to androgen deprivation therapy, castration resistant prostate cancer demands alternative treatment options. It has been reported that the apoptotic protease, caspase 2 (C2) is critical for prostate cancer cell death in several settings. Several reports have also indicated that fatty acid synthesis is critical for maintaining prostate cancer cell viability and that inhibition of fatty acid synthesis can lead to apoptosis. Finally, C2 is suppressed by high intracellular NADPH and this is not due to the redox effects of NADPH, suggesting that the synthetic role of NADPH (e.g., in fatty acid synthesis) may account for its ability to suppress apoptosis. Our new data suggest that manipulating metabolism, particularly inhibiting fatty acid synthesis, can alter chemosensitivity in prostate cancer cells.

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Document Details

Document Type
Technical Report
Publication Date
May 01, 2013
Accession Number
ADA583479

Entities

People

  • Sally Kornbluth

Organizations

  • Duke University

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Androgens
  • Apoptosis
  • Biomedical Research
  • Castration
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemotherapeutic Agents
  • Cultured Cells
  • Deprivation
  • Fatty Acids
  • Inhibition
  • Metabolism
  • Neoplasms
  • Phosphorylation
  • Prostate
  • Prostate Cancer

Fields of Study

  • Biology

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular and Cellular Biochemistry
  • Oncology (Cancer Research).