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

Precision Radiation Oncology

article

Zenan Chen¹  Yanrong Hao¹ 

[1] Cancer Center, People's Hospital of Guangxi Zhuang Autonomous Region;Hubei Provincial Hospital of Traditional Chinese Medicine

关键词: B-cell lymphoma 2;    B-cell lymphoma 2-associated X protein;    beclin 1;    colony-stimulating factor-1 receptor;    nasopharyngeal carcinoma;    sequestosome 1;   

DOI  :  10.1002/pro6.1078

学科分类：社会科学、人文和艺术（综合）

来源: Wiley

【 摘 要 】

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 colonystimulating 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 CSF1R 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.

【 授权许可】

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