The aim of this study was to investigate the effects of the macrophage colony-stimulating factor (M-CSF) receptor antagonist on hepatic carcinogenesis in mice.
Colony-stimulating factor 1 receptor (CSF-1R) and its ligands, CSF-1 and interleukin 34 (IL-34), regulate the function and survival of tumor-associated macrophages, which are involved in tumorigenesis and in the suppression of antitumor immunity.
Overexpression of CSF1 in MCF‑7 fails to rebuild its aggressiveness both in vitro and in vivo since CSF1 was not found extracellularly, while genetic inhibition of CSF1 in MDA‑MB‑231 abrogates TAM infiltration and consequently reduces tumorigenesis in non‑obese diabetic/severe combined immunodeficient (NOD/SCID) mice.
The biologic significance of this translocation is not clear; however, the 1p21 locus is in the region of colony stimulating factor (CSF-1), which may play a role in tumorigenesis, as has been described in pigmented villonodular synovitis and tenosynovial giant cell tumor.
Combined, the data show for the first time the induction of CSF-1 and c-fms in cervical carcinomas and suggest that c-fms activation may play a role in cervical carcinogenesis.