The Role of Inflammation in Breast and Prostate Cancer Metastasis to Bone

Int J Mol Sci. 2021 May 11;22(10):5078. doi: 10.3390/ijms22105078.


Tumor metastasis to bone is a common event in multiple forms of malignancy. Inflammation holds essential functions in homeostasis as a defense mechanism against infections and is a strategy to repair injured tissue and to adapt to stress conditions. However, exaggerated and/or persistent (chronic) inflammation may eventually become maladaptive and evoke diseases such as autoimmunity, diabetes, inflammatory tissue damage, fibrosis, and cancer. In fact, inflammation is now considered a hallmark of malignancy with prognostic relevance. Emerging studies have revealed a central involvement of inflammation in several steps of the metastatic cascade of bone-homing tumor cells through supporting their survival, migration, invasion, and growth. The mechanisms by which inflammation favors these steps involve activation of epithelial-to-mesenchymal transition (EMT), chemokine-mediated homing of tumor cells, local activation of osteoclastogenesis, and a positive feedback amplification of the protumorigenic inflammation loop between tumor and resident cells. In this review, we summarize established and evolving concepts of inflammation-driven tumorigenesis, with a special focus on bone metastasis.

Keywords: bone colonization; cancer; inflammation; metastasis; tumor microenvironment.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone Neoplasms / etiology
  • Bone Neoplasms / secondary*
  • Breast Neoplasms / immunology
  • Breast Neoplasms / pathology*
  • Female
  • Humans
  • Inflammation / complications*
  • Male
  • Prostatic Neoplasms / immunology
  • Prostatic Neoplasms / pathology*
  • Signal Transduction