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Human prostate adenocarcinomas express in-vivo messenger-rnas and protein products for platelet-derived growth

M Xiao1, T Galanopoulos, J Nevillegolden

  • 1HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT UROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115.

International Journal of Oncology
|May 17, 2011
PubMed

Insights

Malignant prostate cells express platelet-derived growth factor B (PDGF-B) and its receptor (PDGF-R) beta, suggesting an autocrine loop driving tumor growth. Nonmalignant cells lack this expression, while androgen receptor mRNA decreases with tumor dedifferentiation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Prostate adenocarcinoma is a common malignancy.
  • The role of growth factors and their receptors in cancer progression is an active area of research.
  • Androgen receptor signaling is crucial in prostate cancer, but its interplay with other pathways is not fully understood.

Purpose of the Study:

  • To investigate the in vivo expression of platelet-derived growth factor B (PDGF-B) and its receptor beta (PDGF-R beta) in human prostatic adenocarcinomas.
  • To compare the expression of PDGF-B and PDGF-R beta in malignant versus nonmalignant prostate tissues.
  • To assess the expression of androgen receptor mRNA in relation to tumor differentiation.

Main Methods:

  • In situ hybridization was used to detect PDGF-B, PDGF-R beta, and androgen receptor mRNAs.
  • Immunocytochemistry was employed to identify the respective protein products.
  • Expression levels were analyzed in eight primary human prostatic adenocarcinomas and five adjacent nonmalignant prostate tissues.

Main Results:

  • PDGF-B and PDGF-R beta mRNAs and proteins were expressed in malignant epithelial cells of prostatic adenocarcinomas.
  • Significant expression of PDGF-B and PDGF-R beta was not detected in nonmalignant prostate epithelial cells.
  • Androgen receptor mRNA was present in nonmalignant tissues but showed reduced expression in both well-differentiated and poorly differentiated malignant regions, with a more pronounced reduction in poorly differentiated areas.

Conclusions:

  • Coexpression of PDGF-B and PDGF-R beta in malignant prostate epithelial cells suggests an autocrine signaling loop that may promote tumor growth and maintenance.
  • The observed reduction in androgen receptor mRNA expression correlates with tumor dedifferentiation in prostatic adenocarcinomas.
  • These findings highlight a potential therapeutic target involving the PDGF signaling pathway in prostate cancer.

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