Characterization of Putative Homeostatic Molecules in Prostate Development and Androgen-Independent Prostate Cancer

Abstract

The goal of this study to define the signal pathway(s) elicited by two homeostatic genes, C-CAM1 and DOC-2, in the basal cells of normal prostate. Prostate basal cells have been shown to have similar biologic properties to the androgen-independent (AI) prostate cancer. The outcome of this study can improve the current treatment strategy for AI prostate cancer. structurally, C-CAM1 is a cell adhesion molecule with receptor kinase motif in the C-terminus. Together with DOC-2, a typical signal molecule, we believe that both genes play an important role in controlling the growth and differentiation of prostatic epithelia. Our results indicate that both C-CAM1 and DOC-2 are down-regulated in Al prostate cancer and increased expression of individual gene can inhibit cancer growth. We have further defined the functional domain in both genes which modulate their tumor suppression activities. More detailed analyses are underway for C-CAM1 protein. For DOC-2 protein, it appears that DOC-2 can interact with an novel protein that belongs to the Ras GTPase-activating protein (GAP) family. Ras-GAP is a key factor to maintain the balance of both active and inactive status of Ras protein. Our finding signifies the critical role of DOC-2 in prostate development and carcinogenesis.

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Document Details

Document Type
Technical Report
Publication Date
Jan 01, 2000
Accession Number
ADA385421

Entities

People

  • Jer-tsong Heleh

Organizations

  • University of Texas Southwestern Medical Center

Tags

DTIC Thesaurus Topics

  • Adhesion
  • Amino Acids
  • Androgens
  • Biomedical Research
  • Blood
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemistry
  • Epithelial Cells
  • Epithelium
  • Medical Personnel
  • Molecules
  • Neoplasms
  • Polymerase Chain Reaction
  • Prostate Cancer
  • Tissues

Readers

  • Marine Ecotoxicology
  • Molecular Biology and Genetics
  • Prostate Cancer Biology.