All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Abstract

Sulfamethoxazole Inhibit Lung Adenocarcinoma-Derived Exosomes Induced M2-Type Macrophage Polarization

Author(s): Q. Dong, Junyu Luo, Lanlan Liu, Rong Zhao, X. Li and Y. Luan*
College of Acupuncture, Moxibustion and Tuina, Yunnan University of Traditional Chinese Medicine, Kunming 650500, 1Department of Clinical Laboratory, The First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming 650021, 2Engineering Research Center for Inheritance And Innovation of Traditional Chinese Medicine, The First Affiliated Hospital of Yunnan University of Traditional Chinese Medicine, Kunming 650034, 3Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, Southwest Forestry University, Kunming 650224, China

Correspondence Address:
Y. Luan, Key Laboratory for Forest Resources Conservation and Utilization in the Southwest Mountains of China, Ministry of Education, Southwest Forestry University, Kunming 650224, China, E-mail: LuanTeam@163.com


Sulfamethoxazole suppress the secretion of exosomes from tumors, however its roles in modulation of proliferation, invasion and metastasis of adenocarcinoma cells, and tumor associated macrophages polarization remained unclear, therefore this study was carried on to elaborate the mechanisms. Exosomes of lung adenocarcinoma cell line A549 were extracted by ultracentrifugation; sulfamethoxazole was added and identified by Western blot method. The expression levels of surface markers of M1-type and M2-type macrophages were detected by quantitative polymerase chain reaction. A549 cells were cocultured with polarized M2-type macrophages, and the proliferation and migration ability of A549 cells was examined by cell counting kit-8 and scratch assays. Western blot was used to detect the expression of phosphoinositide-3-kinase, phospho-phosphoinositide-3-kinase, protein kinase B and phospho-protein kinase B. Animal experiments showed that lung adenocarcinoma-derived exosomes could promote the growth of tumor by the polarization of M2-type macrophages, and identification of lung adenocarcinomaderived exosomes by the addition of sulfamethoxazole and exosomes. Lung adenocarcinoma-derived exosomes were activated by phosphoinositide-3-kinase/protein kinase B signaling pathway to promote the polarization of M2-type macrophages to enhance the proliferation and migration of cancer cells. In addition, lung adenocarcinoma-derived exosomes can promote tumor growth in a subcutaneous mouse tumor model. Lung adenocarcinoma-derived exosomes promote the polarization of M2-type macrophages and promote the development of lung cancer through phosphatidylinositol-3-kinase/ protein kinase B signaling pathway.

Full-Text | PDF

 
 
Google scholar citation report
Citations : 61564

Indian Journal of Pharmaceutical Sciences received 61564 citations as per google scholar report