Bone marrow-derived cells and epithelial tumours: more than just an inflammatory relationship.

ABSTRACT

PURPOSE OF REVIEW Cancer-associated fibroblasts/myofibroblasts and inflammatory cells produce a vast array of growth factors, chemokines and extracellular matrix (ECM) components that facilitate cancer progression, invasion/metastasis and neovascularization. This review highlights some surprisingly novel mechanisms of this paracrine relationship. RECENT FINDINGS: Mesenchymal stem/stromal cells (MSCs) are known for their tropism towards certain tumours, but now we find that cross-talk between tumours and MSCs leads to greater tumour motility and metastasis. Two closely related populations of immature myeloid cells, so-called 'cap cells' and myeloid-derived suppressor cells (MDSCs) also cross-talk with tumour cells, promoting invasion and metastasis through matrix metalloproteinase (MMP) secretion, as well as contributing to neovascularization and T-cell tolerance. The contribution of bone marrow-derived cells (BMDCs) to tumour neovascularization is controversial, but BMD--endothelial progenitor cells (EPCs)--are strongly implicated in the angiogenic switch in a mouse model. BMDCs are also credited with the creation of premetastatic niches to which metastatic cells adhere via integrins. SUMMARY: There is no doubt that BMDCs are not simply bystanders in the tumour battleground. The mechanisms through which they aid tumour progression are numerous; effective treatments that combat BMDC-tumour cross-talk are surely on the way.