Role of TGF-beta in Prostate Cancer Progression

Abstract

There is strong evidence that inflammation and interactions with the surrounding stromal microenvironment are critical for cancer initiation and progression. As a major component of the stroma, fibroblasts are recognized as prominent modifiers of cancer progression. The contribution of carcinoma associated fibroblasts (CAF) to cancer has been approved and become accepted, research has been conducted to understand the mechanisms underlying this stromal-epithelial interaction. In this project we have demonstrated that relatively small changes in the expression levels of TGFbeta and SDF1/CXCL12 in human prostate cancer stromal cells can drive carcinogenesis in human prostatic epithelium. In two publications we showed linkage between the two pathways in that TGFbeta elevates CXCR4, the cognate receptor for SDF1, in the epithelial cells allowing activation of the SDF signaling pathway. This in turn activates Akt phosphorylation which is sufficient to suppress the growth inhibitory response to TGFbeta. This link provides a mechanism for the switch in TGFbeta activity from growth suppressive in normal tissue to growth promoting in cancer and suggests routes for therapeutic intervention.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2008
Accession Number
ADA502784

Entities

People

  • Mingfang Ao

Organizations

  • Vanderbilt University Medical Center

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Cancer
  • Cells
  • Epithelial Cells
  • Epithelium
  • Fibroblasts
  • Growth Factors
  • Medical Personnel
  • Neoplasms
  • Peptide Growth Factors
  • Prostate
  • Prostate Cancer
  • Tissues

Fields of Study

  • Medicine

Readers

  • Molecular Biology and Genetics