Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/ijms22105078
Keywords
inflammation; metastasis; cancer; bone colonization; tumor microenvironment
Funding
- Deutsche Forschungsgemeinschaft [SPP-2084]
- Deutsche Krebshilfe as part of the Mildred Scheel Early Career Center
- Publication Fund of the TU Dresden
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Inflammation plays a critical role in bone metastasis by supporting the survival, migration, invasion, and growth of tumor cells, serving as a key factor in the tumorigenesis and progression of cancer.
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.
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