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How to Study Basement Membrane Stiffness as a Biophysical Trigger in Prostate Cancer and Other Age-related Pathologies or Metabolic Diseases
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How to Study Basement Membrane Stiffness as a Biophysical Trigger in Prostate Cancer and Other Age-related Pathologies or Metabolic Diseases

Published on: September 20, 2016

Relaxin promotes prostate cancer progression.

Shu Feng1, Irina U Agoulnik, Natalia V Bogatcheva

  • 1Department of Obstetrics and Gynecology, Molecular and Cellular Biology, and Pathology, Baylor College of Medicine, Houston, TX 77030, USA.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
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Relaxin peptide promotes prostate cancer progression by increasing cell proliferation and invasiveness. Inhibiting relaxin signaling significantly reduced cancer growth and improved apoptosis, suggesting it as a therapeutic target.

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Area of Science:

  • Oncology
  • Endocrinology
  • Molecular Biology

Background:

  • Relaxin peptide's role in prostate cancer is not fully understood.
  • Investigating relaxin and its receptor (LGR7) in prostate cancer is crucial for therapeutic development.

Purpose of the Study:

  • To determine the expression of relaxin and LGR7 in prostate cancer.
  • To analyze the impact of relaxin signaling on prostate cancer cell behavior in vitro.
  • To evaluate the effect of elevated relaxin on cancer progression in vivo.

Main Methods:

  • Quantitative RT-PCR and immunohistochemistry for relaxin/LGR7 expression in human prostate tissues.
  • In vitro studies using PC-3 and LNCaP cells treated with relaxin or short interfering RNA (siRNA).
  • In vivo studies using transgenic adenocarcinoma of the mouse prostate (TRAMP) model with relaxin overexpression.

Main Results:

  • Relaxin mRNA expression was higher in recurrent prostate cancer.
  • Relaxin stimulation increased prostate cancer cell proliferation, invasiveness, and adhesion.
  • siRNA suppression of relaxin/LGR7 reduced invasiveness and growth, while increasing apoptosis.
  • Transgenic mice with relaxin overexpression showed reduced survival due to decreased tumor cell apoptosis.

Conclusions:

  • Relaxin signaling is implicated in prostate cancer progression.
  • Targeting relaxin/LGR7 signaling may offer a therapeutic strategy for prostate cancer.