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Dysregulation of Dkk-3 expression in benign and malignant prostatic tissue

Christoph Zenzmaier1, Gerold Untergasser, Martin Hermann

  • 1Institute for Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria.

The Prostate
|February 6, 2008
PubMed
Abstract

Insights

Dickkopf-3 (Dkk-3) expression is lost in prostate cancer epithelial cells but upregulated in blood vessels. This suggests Dkk-3

Area of Science:

  • Urology
  • Oncology
  • Molecular Biology

Background:

  • The Dickkopf (Dkk) family has four members, with Dkk-3 being the most divergent and not modulating Wnt signaling.
  • Dkk-3 is proposed as a secreted tumor suppressor due to its downregulation in various cancers, including prostate cancer.
  • This downregulation suggests Dkk-3's potential as a therapeutic target in prostate cancer treatment.

Purpose of the Study:

  • To investigate the in situ tissue localization of Dkk-3 protein in normal prostate (NP), benign prostatic hyperplasia (BPH), and prostate carcinoma (PCa).
  • To evaluate the biological function of Dkk-3 on proliferation and viability in prostate cells.
  • To explore Dkk-3's role in prostate cancer development and progression.

Main Methods:

  • Immunohistochemistry (IHC)/immunofluorescence for Dkk-3 protein localization.
  • In vitro studies using recombinant Dkk-3 protein or overexpression in primary prostate cells and PCa cell lines.
  • Assessment of cell proliferation and viability upon Dkk-3 treatment or overexpression.

Main Results:

  • Dkk-3 protein expression was observed in the basal and secretory epithelium of normal prostate tissue.
  • Dkk-3 expression was lost in high-grade PCa tumor cells but restricted to basal cells in BPH.
  • Upregulation of Dkk-3 was noted in subglandular blood vessels of BPH and reactive stroma of PCa.

Conclusions:

  • Prostate Dkk-3 expression in the epithelium is lost during benign and malignant transformation.
  • This loss of epithelial Dkk-3 expression is counterbalanced by its upregulation in the blood vessels of remodeled prostate tissue.
  • Dkk-3's differential expression suggests a complex role in prostate tissue remodeling and cancer progression.

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