Loss of inhibition over master pathways of bone mass regulation results in osteosclerotic bone metastases in prostate cancer

Swiss Med Wkly. 2009 Apr 18;139(15-16):220-5. doi: 10.4414/smw.2009.12284.

Abstract

Prostate cancer is the most common cancer among men in industrialised countries. Most patients with prostate cancer, however, will not die of it. As a result, many of them will experience symptomatic metastasis during the course of the disease. Prostate cancer has a high propensity to metastasize to bone. Unlike many other cancers prostate cancer cells induce a rather osteosclerotic than osteolytic reaction in the bone marrow by interfering with physiological bone remodelling. A proper understanding of the mechanisms of tumour cell-induced bone alterations and exaggerated bone deposition in prostate cancer may open new and urgently needed therapeutic approaches in the field of palliative care for affected patients. In this review we focus on the central role of two major regulators of bone mass, the wingless type integration site family members (WNTs) and the bone morphogenetic proteins (BMPs), in the development of osteosclerotic bone metastases.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone Morphogenetic Proteins / antagonists & inhibitors
  • Bone Morphogenetic Proteins / physiology*
  • Bone Neoplasms / physiopathology*
  • Bone Neoplasms / secondary*
  • Bone Remodeling / physiology
  • Carrier Proteins / pharmacology
  • Humans
  • Male
  • Models, Animal
  • Osteoblasts / physiology
  • Osteosclerosis / etiology
  • Osteosclerosis / pathology
  • Osteosclerosis / physiopathology*
  • Prostatic Neoplasms / pathology*
  • Signal Transduction / physiology*
  • Wnt Proteins / physiology*

Substances

  • Bone Morphogenetic Proteins
  • Carrier Proteins
  • Wnt Proteins
  • noggin protein