Background: The relation between the expression of macrophage-colony stimulating factor-1 receptor (CSF-1R) and prognosis of cancer patients has been evaluated in multiple studies, but the results remain controversial. We, therefore, performed a meta-analysis and systematic review to figure out the role of CSF-1R in the prognosis of patients with cancer. Methods: Several databases were searched, including Web of Science, PubMed, and EMBASE. All human studies were published as full text. The Newcastle–Ottawa risk of bias scale was applied to evaluate the research. We extracted hazard ratios (HRs) with 95% confidence interval (95% CI) which assessed progression-free survival (PFS) and overall survival (OS) in order to assess the impacts of CSF-1R on the prognosis of cancer patients. Results: A total of 12 citations were identified, with studies including 2260 patients in different cancer types that met the eligibility criteria. It was suggested in a pooled analysis that the over-expression of CSF-1R was significantly related to worse PFS (HR: 1.68; P < .001, 1.25–2.10, 95% CI) and also poorer OS (HR=1.28; P < .001, 1.03–1.54, 95% CI). Analysis in subgroups indicated over-expressed CSF-1R was significantly associated with worse OS in hematological malignancy (HR = 2.29; P < .001, 1.49–3.09, 95% CI; model of fixed-effects; I 2 = 0.0%, P < .001). Sensitivity analysis suggested that there was no study influencing the stability of the results. Conclusions: The overexpression of CSF-1R was significantly predictive of worse prognosis in those who suffer from different kinds of malignancies, particularly in hematological malignancy, which indicates that it might be a potential biomarker of prognosis in cancer survival and a potential molecular target in the treatment of malignant tumors.

Objectives In nasopharyngeal carcinoma (NPC), the main factors for treatment failure are local recurrence and metastasis. Vasculogenic mimicry (VM), formation by invasive cancer cells mimicking the vasculogenic network, is strongly correlated with tumor therapy resistance and distant metastasis. CSF-1R was substantially expressed in NPC patients with a poor prognosis, according to an earlier study of ours. However, whether CSF-1R affects progression through vasculogenic mimicry deserves consideration. Methods By cultivating NPC cells that had CSF-1R overexpression in three-dimensional culture and labeling the NPC xenografts with CD34-PAS vasculogenic mimicry markers, the effect of CSF-1R on VM formation, migration, and invasion of NPC cells was evaluated. Finally, the underlying mechanisms were investigated by western blot. Results In vitro and in vivo, overexpressing CSF-1R in NPC cells causes the development of vessel-like structures. Meanwhile, NPC cells migrated and invaded more readily in the Transwell experiment when CSF-1R was highly expressed. Mechanistically, our research indicates that CSF-1R may control cell plasticity by activating the PI3K/AKT signaling pathway, promoting the formation of VM in these cells by facilitating the epithelial-mesenchymal transition. Conclusions CSF-1R in NPC progression by increasing VM production to increase nutrient supply to tumor cells and promote cancer cell invasion. Furthermore, these findings suggest that CSF-1R is a new promising therapeutic target aimed at treating VM in NPC.