Co-Operation Between FADD and Bin1 in Prostate Cancer Apoptosis

Abstract

This project studies a novel apoptosis pathway that is induced by the death domain of the adaptor protein FADD (FADD-DD). The current project is based on preliminary data showing that the tumor suppressor Bin1 can co-operate with FADD-DD to kill a prostate tumor cell line (LNCaP) that is normally resistant to FADD-DD. The Pi's laboratory has moved from Wake Forest University to the University of Colorado (UCHSC) and we requested that the award be transferred to UCHSC so that this work may continue. This report covers the period between the previous progress report and the move to UCHSC (April 1 2004- Sept. 1 2004) . In this funding period, we continued to achieve the goals outlined in the approved statement of work and are still ahead of our original schedule. We demonstrated that other prostate cell lines do not behave -the same way indicating that the Bin1-deficiency is not the only way that tumor cells can subvert this pathway. In addition other experiments were performed which show that the mechanism of tumor cell death by FADD-DD pathway Involves autophagy as well as apoptosis. These extra studies allow new avenues of research to be explored in the next funding period.

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Document Details

Document Type
Technical Report
Publication Date
Apr 01, 2005
Accession Number
ADA439128

Entities

People

  • Andrew M. Thorburn

Organizations

  • Wake Forest University

Tags

DTIC Thesaurus Topics

  • Apoptosis
  • Autophagy
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Electron Microscopy
  • Epithelial Cells
  • Mammary Glands
  • Microscopy
  • Molecular Biology
  • Neoplasms
  • Programmed Cell Death
  • Prostate
  • Prostate Cancer
  • Tissues
  • Tumor Cell Line

Readers

  • Cellular and Molecular Pathways of Apoptosis.
  • Molecular Biology and Genetics
  • Research Science/Academic Research