Sphingolipid-Mediated Apoptosis and Tumor Suppression in Breast Carcinoma.

Abstract

Ceramide has emerged as an important intracellular regulator of cell growth and viability. In breast carcinoma cells, we find that tumor necrosis factor a (TNFa) causes prolonged and significant accumulation of ceramide, which precedes cell death. We have investigated the mechanism of ceramide formation and the mechanism of ceramide action, with specific emphasis on their interactions with proteases. Our studies lead us to define two phases of the apoptotic pathway: in the first, signaling phase, TNFa: causes activation of proteases which lead to the accumulation of ceramide. In the second, execution phase, ceramide causes the activation of downstream death proteases as well as activation of the retinoblastoma gene product. Addition of exogenous ceramides causes simultaneously cell cycle arrest and cell death. These studies are beginning to identify a growth suppressor pathway in breast carcinoma cells and the results are beginning to interrelate important components involved in the apoptotic response.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 1996
Accession Number
ADB221779

Entities

People

  • Yusuf A. Hannun

Organizations

  • Duke University Hospital

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Biological Factors
  • Biomedical Research
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Chemotherapeutic Agents
  • Fungi
  • Materials
  • Neoplasms
  • Programmed Cell Death
  • Proteins
  • Tumor Cell Line

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular Biology and Genetics