The impact of cell adhesion changes on proliferation and survival during prostate cancer development and progression

J Cell Biochem. 2006 Oct 1;99(2):345-61. doi: 10.1002/jcb.20934.

Abstract

In the normal prostate epithelium, androgen receptor (AR) negative basal epithelial cells adhere to the substratum, while AR expressing secretory cells lose substratum adhesion. In contrast, prostate cancer cells both express AR and adhere to a tumor basement membrane. In this review, we describe the differential expression of integrins, growth factor receptors (GFRs), and AR in normal and cancerous epithelium. In addition, we discuss how signals from integrins, GFRs, and AR are integrated to regulate the proliferation and survival of normal and malignant prostate epithelial cells. While cell adhesion is likely of great importance when considering therapeutic approaches for treatment of metastatic prostate cancer, no data on integrin expression are available from tissues of prostate cancer metastasis. However, several drug targets that are upregulated after androgen ablative therapy regulate cell adhesion and thus novel targeted therapies indirectly interfere with cell adhesion mechanisms in prostate cancer cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Androgen Antagonists / therapeutic use
  • Androgens / physiology
  • Animals
  • Cell Adhesion / physiology*
  • Cell Proliferation
  • Cell Survival / physiology
  • Epithelial Cells / cytology
  • Epithelial Cells / physiology
  • Extracellular Matrix Proteins / physiology
  • Humans
  • Integrins / physiology
  • Intercellular Signaling Peptides and Proteins / physiology
  • Male
  • Models, Biological
  • Neoplasm Invasiveness
  • Neoplasms, Hormone-Dependent / drug therapy
  • Neoplasms, Hormone-Dependent / etiology
  • Neoplasms, Hormone-Dependent / pathology
  • Neoplasms, Hormone-Dependent / physiopathology
  • Prostate / cytology
  • Prostate / physiology
  • Prostatic Neoplasms / drug therapy
  • Prostatic Neoplasms / etiology*
  • Prostatic Neoplasms / pathology*
  • Prostatic Neoplasms / physiopathology
  • Receptor Cross-Talk
  • Receptors, Growth Factor / physiology
  • Signal Transduction

Substances

  • Androgen Antagonists
  • Androgens
  • Extracellular Matrix Proteins
  • Integrins
  • Intercellular Signaling Peptides and Proteins
  • Receptors, Growth Factor