Effect of colony‐stimulating factor‐1 receptor overexpression on the growth of nasopharyngeal carcinoma xenografts in nude mice and its mechanism of action

Objectives Although nasopharyngeal carcinoma (NPC) is sensitive to radiotherapy, local recurrence and distant metastasis still occur in a proportion of patients due to radioresistance. Our previous research confirmed that colony‐stimulating factor‐1 receptor (CSF‐1R) promotes the proliferation, migration, and invasion of 6‐10B cells through the phosphoinositide 3‐kinase (PI3K) pathway in vitro . The objective of the present study was to investigate the effects of colony‐stimulating factor‐1 receptor (CSF‐1R) on proliferation, apoptosis, and autophagy in the human nasopharyngeal carcinoma 6‐10B cell line in vivo , and the possible underlying mechanisms. Methods A virus carrying the CSF‐1R gene was transfected into 6‐10B cells by lentiviral transfection. A nasopharyngeal carcinoma xenograft model in nude mice was established. Ultimately, the protein expression of proliferation‐, apoptosis‐, autophagy‐, and signaling‐related proteins, such as cyclin D1, B‐cell lymphoma 2 (Bcl‐2), Bcl‐2‐associated X protein, beclin 1, microtubule‐associated protein 1 light chain 3 alpha, sequestosome 1, mechanistic target of rapamycin kinase, PI3K, and protein kinase B (Akt/PKB), in tumor tissues were detected by western blot analysis. Results High levels of CSF‐1R were expressed in the stably transfected 6‐10B cells, while CSF‐1R promoted the growth of 6‐10B cells in vivo . Cyclin D1, Bcl‐2, microtubule‐associated protein 1 light chain 3 alpha, and beclin 1 were upregulated, while Bcl‐2‐associated X protein and sequestosome 1 were downregulated. Furthermore, the expression of PI3K, phospho‐Akt, Akt, and mechanistic target of rapamycin kinase were upregulated. Conclusions CSF‐1R overexpression promotes proliferation, reduces apoptosis, and induces autophagy in 6‐10B cells in vivo , and the corresponding mechanism might be executed through activation of the PI3K/Akt pathway.