Jie Lei1, Peng Chen1, Feng Zhang2, Na Zhang1, Jianfei Zhu1, Xiaoping Wang3, Tao Jiang4. 1. Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, 569 Xin Si Road, Xi'an, 710038, Shanxi, China. 2. Department of Oncology, The Second Affiliated Hospital of Air Force Medical University, Xi'an, 710038, Shanxi, China. 3. Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, 569 Xin Si Road, Xi'an, 710038, Shanxi, China. Wangxiaoping7456@163.com. 4. Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, 569 Xin Si Road, Xi'an, 710038, Shanxi, China. Jiangtao4153@163.com.
Abstract
BACKGROUND: Exosomes are known to transmit microRNAs (miRNAs) to affect cancer progression, while the role of M2 macrophages-derived exosomes (M2 exosomes) conveying miR-501-3p in lung cancer (LC) remains unknown. We aim to explore the role of exosomal miR-501-3p in LC development via targeting WD repeat domain 82 (WDR82). METHODS: Lung cancer tissue and normal tissue specimens were collected, in which tumor-associated macrophages (TAM) were measured by immunohistochemistry. M2 macrophages were induced and treated with altered miR-501-3p, and then the exosomes were extracted and identified. MiR-501-3p and WDR82 expression in LC tissues and cell liens was determined. The predictive role of miR-501-3p in prognosis of LC patients was assessed, and the proliferation, colony formation ability, invasion, migration and apoptosis of the LC cells were determined. Targeting relationship between miR-501-3p and WDR82 was confirmed. RESULTS: TAM level was elevated in lung cancer tissues. MiR-501-3p was upregulated while WDR82 was downregulated in LC tissues and cell lines, and the M2 exosomes further upregulated miR-501-3p. M2 exosomes and exosomal miR-501-3p promoted LC cell growth. MiR-501-3p inhibition reversed the effect of M2 exosomes on LC cells. WDR82 was confirmed as a target gene of miR-501-3p. CONCLUSION: M2 macrophages-derived exosomal miR-501-3p promotes the progression of LC via downregulating WDR82.
BACKGROUND: Exosomes are known to transmit microRNAs (miRNAs) to affect cancer progression, while the role of M2 macrophages-derived exosomes (M2 exosomes) conveying miR-501-3p in lung cancer (LC) remains unknown. We aim to explore the role of exosomal miR-501-3p in LC development via targeting WD repeat domain 82 (WDR82). METHODS:Lung cancer tissue and normal tissue specimens were collected, in which tumor-associated macrophages (TAM) were measured by immunohistochemistry. M2 macrophages were induced and treated with altered miR-501-3p, and then the exosomes were extracted and identified. MiR-501-3p and WDR82 expression in LC tissues and cell liens was determined. The predictive role of miR-501-3p in prognosis of LC patients was assessed, and the proliferation, colony formation ability, invasion, migration and apoptosis of the LC cells were determined. Targeting relationship between miR-501-3p and WDR82 was confirmed. RESULTS:TAM level was elevated in lung cancer tissues. MiR-501-3p was upregulated while WDR82 was downregulated in LC tissues and cell lines, and the M2 exosomes further upregulated miR-501-3p. M2 exosomes and exosomal miR-501-3p promoted LC cell growth. MiR-501-3p inhibition reversed the effect of M2 exosomes on LC cells. WDR82 was confirmed as a target gene of miR-501-3p. CONCLUSION: M2 macrophages-derived exosomal miR-501-3p promotes the progression of LC via downregulating WDR82.
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