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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Disruption of growth hormone signaling retards prostate carcinogenesis in the Probasin/TAg rat

Zhuohua Wang1, Raul M Luque, Rhonda D Kineman

  • 1Department of Medicinal Chemistry and Pharmacognosy, Univeresity od Illinois at Chicago, Chicago, Illinois 60612-7231.

Endocrinology
|December 15, 2007
PubMed

Insights

Down-regulating growth hormone (GH) signaling significantly reduced prostate cancer progression in a rat model. Loss of GH delayed tumor development and decreased tumor burden, suggesting GH antagonists may treat human prostate cancer.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Prostate cancer is a significant health concern.
  • The role of growth hormone (GH) in prostate cancer progression is not fully understood.
  • The Probasin/TAg rat is a model for aggressive prostate cancer.

Purpose of the Study:

  • To investigate if down-regulating GH signaling can inhibit prostate carcinogenesis.
  • To determine the effect of GH deficiency on prostate tumor development and progression in the Probasin/TAg rat model.

Main Methods:

  • Crossed Spontaneous Dwarf rats (GH-deficient) with Probasin/TAg rats.
  • Compared prostate tumor incidence, burden, and latency in GH-deficient (TAg/Gh(dr/dr)) and control (TAg/Gh(+/+)) rats.
  • Analyzed prostate expression of GH receptor (GHR), IGF-I receptor, TAg, and androgen receptor, as well as serum testosterone and IGF-I levels.

Main Results:

  • GH deficiency significantly reduced prostate tumor incidence and burden, and delayed tumor latency.
  • Loss of GH led to a marked decrease in microinvasive carcinoma area in dorsal and lateral prostate lobes.
  • While invasive adenocarcinomas developed in all controls, the majority of GH-deficient rats did not develop invasive tumors by 52 weeks.
  • GH deficiency did not alter TAg or androgen receptor expression or serum testosterone levels.
  • Prostate GHR expression increased, while IGF-I receptor expression decreased during carcinogenesis in control rats.

Conclusions:

  • GH plays a dominant role in the progression of prostate cancer from latent to malignant stages in this rat model.
  • GH signaling suppression effectively inhibits prostate carcinogenesis.
  • GH antagonists represent a potential therapeutic strategy for human prostate cancer.

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