Pathogenesis of osteoblastic bone metastases from prostate cancer

Toni Ibrahim, Emanuela Flamini, Laura Mercatali, Emanuele Sacanna, Patrizia Serra, Dino Amadori

Research output: Contribution to journalArticlepeer-review


Prostate cancer is the second leading cause of cancer-related death in men. A typical feature of this disease is its ability to metastasize to bone. It is mainly osteosclerotic, and is caused by a relative excess of osteoblast activity, leading to an abnormal bone formation. Bone metastases are the result of a complex series of steps that are not yet fully understood and depend on dynamic crosstalk between metastatic cancer cells, cellular components of the bone marrow microenvironment, and bone matrix (osteoblasts and osteoclasts). Prostate cancer cells from primary tissue undergo an epithelial-mesenchymal transition to disseminate and acquire a bone-like phenotype to metastasize in bone tissue. This review discusses the biological processes and the molecules involved in the progression of bone metastases. Here we focus on the routes of osteoblast differentiation and activation, the crosstalk between bone cells and tumor cells, and the molecules involved in these processes that are expressed by both osteoblasts and tumor cells. Furthermore, this review deals with the recently elucidated role of osteoclasts in prostate cancer bone metastases. Certainly, to better understand the underlying mechanisms of bone metastasis and so improve targeted bone therapies, further studies are warranted to shed light on the probable role of the premetastatic niche and the involvement of cancer stem cells.

Original languageEnglish
Pages (from-to)1406-1418
Number of pages13
Issue number6
Publication statusPublished - Mar 15 2010


  • Bone
  • Metastasization
  • Osteoblasts
  • Osteoclasts
  • Prostate cancer

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


Dive into the research topics of 'Pathogenesis of osteoblastic bone metastases from prostate cancer'. Together they form a unique fingerprint.

Cite this