Its expression is also detected in some cancers but its role in cancer cell biology is not fully recognized. Data reported in the literature indicated that the oncogenic potential of CSF-1R is due to co-expression of this receptor and its ligand CSF-1 (colony stimulating factor-1) in epithelial cancer cells, or mutations activating CSF-1R independently of ligand. Activation of CSF-1R by its ligand is likely to occur in an autocrine manner in tumor cells in which CSF-1R and CSF-1 are co-expressed, or in paracrine manner, when CSF-1R is stimulated by CSF-1 released by fibroblasts. However, our recent studies have shown that CSF-1R in cancer cells can be stimulated by colony stimulating factor secreted by tumor-associated macrophages. Interestingly, we showed that their co-culture leads to up-regulation of CSF in macrophages and up-regulation of CSFs and CSF-1R in cancer cells. These results are in accordance with the observations that CSF-1R is important for cancer metastasis but only in the presence of macrophages. Moreover, our previous study has shown that the expression of CSF-1R in neoplastic epithelial cells of canine mammary gland strongly correlates with grade of malignancy and ability to metastasis. This study was therefore designed to characterize the role of CSF-1R in canine mammary cancer cells proliferation, apoptosis, migration, and invasion.
Król M, Majchrzak K, Mucha J, et al. CSF-1R as an inhibitor of apoptosis and promoter of proliferation, migration and invasion of canine mammary cancer cells. BMC Veterinary Research. 2013;9:65.