CSF-1R promotes vasculogenic mimicry via epithelial-mesenchymal transition in nasopharyngeal carcinoma cells

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