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Updated: Sep 29, 2026

Microarray-based Identification of Individual HERV Loci Expression: Application to Biomarker Discovery in Prostate Cancer
13:19

Microarray-based Identification of Individual HERV Loci Expression: Application to Biomarker Discovery in Prostate Cancer

Published on: November 2, 2013

Expression of growth hormone-releasing hormone and its receptor splice variants in human prostate cancer

Gabor Halmos1, Andrew V Schally, Tamas Czompoly

  • 1Endocrine, Polypeptide, and Cancer Institute, Veterans Affairs Medical Center, and Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.

The Journal of Clinical Endocrinology and Metabolism
|October 5, 2002
PubMed

Insights

Growth hormone-releasing hormone (GHRH) antagonists may fight prostate cancer by targeting tumor cell receptors. This study identified GHRH and its receptor splice variants in prostate tumors, suggesting a local GHRH system that antagonists can disrupt.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Growth hormone-releasing hormone (GHRH) antagonists show promise in inhibiting human tumor growth, including prostate cancer.
  • The specific tumor receptors mediating this effect remain largely unidentified.
  • Previous research indicated that cancer cell lines express GHRH receptor splice variants (SVs), with SV1 being most similar to pituitary receptors.

Purpose of the Study:

  • To investigate the expression of GHRH and its splice variants (SVs) of the GHRH receptor in human prostate cancer specimens.
  • To characterize the binding properties of the GHRH receptor isoform in these tumors.
  • To explore the potential role of a local GHRH system in prostate cancer proliferation.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect mRNA expression of GHRH and GHRH receptor SVs.
  • Ligand competition assays using radiolabeled GHRH antagonist JV-1-42 were performed on tumor membranes to determine receptor affinity and density.
  • Analysis included 20 surgical specimens of organ-confined and locally advanced prostatic adenocarcinomas.

Main Results:

  • Specific, high-affinity binding for the GHRH antagonist JV-1-42 was observed in 60% of tumors (12/20), with a mean K(d) of 0.81 nmol/L and mean B(max) of 185.2 fmol/mg.
  • GHRH receptor SV1 mRNA was detected in 65% of specimens (13/20), correlating with GHRH binding.
  • GHRH receptor mRNA was found in 86% of examined prostate cancer specimens (13/15).

Conclusions:

  • Prostate cancers express both GHRH and its tumor receptor splice variants.
  • The presence of this local GHRH system suggests a potential autocrine mitogenic loop.
  • GHRH antagonists may exert their antitumor effects in prostate cancer partly by interfering with this identified local GHRH system.

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