Activation of the IL-4/STAT6 Signaling Pathway Promotes Lung Cancer Progression by Increasing M2 Myeloid Cells.

Emerging evidence shows that signal transducer and activator of transcription 6 plays critical roles in tumor development. We previously found high-level expression of in human lung adenocarcinoma and squamous cell carcinoma, specifically in infiltrated immune cells located in the lung interstitium. Nevertheless, the role of duanyu18136 signaling in lung carcinogenesis and lung cancer proliferation and its underlying mechanisms remain unclear. This study aimed to investigate the role of duanyu18136 and the interaction between duanyu18136 and the tumor microenvironment in pulmonary tumorigenesis. We established a murine model of primary lung carcinogenesis in and duanyu18136 wild-type (WT) BALB/c mice using the carcinogen urethane. Two-month-old male mice were intraperitoneally injected with urethane (1 g/kg) dissolved in phosphate buffered saline (PBS). Primary tumors were monitored in vivo by positron emission tomography scanning. At 4, 6, and 9 months after urethane injection, lung tumors were harvested from the and WT mice for analysis. Small interfering RNA was used to downregulate the expression of in tumor cells. Fluorescence activated cell sorting analysis was used to analyze fluorescence-conjugated cell markers. Transwell assays were used in coculturing experiments. duanyu18136 protein expression was detected by Western blotting, immunohistochemistry, and immunofluorescence. duanyu18136 mRNA expression was detected by quantitative real time-polymerase chain reaction. Cell Counting Kit-8 and colony formation assays were performed to evaluate cell proliferation. We detected high expression of duanyu18136 in CD11b⁺ cells of lung carcinoma. Our results indicate that duanyu18136 deficiency inhibits carcinogen-induced tumor growth and improves prognosis. duanyu18136 deficiency also decreased the mobilization and differentiation of CD11b⁺ cells. duanyu18136 deficiency in CD11b⁺ cells but not tumor cells decreased interleukin (IL)-4 secretion and the differentiation of CD11b⁺ cells into M2 macrophage cells. In conclusion, our findings indicate that signaling in CD11b⁺ cells promotes lung cancer progression by triggering an IL-4 positive feedback loop and increasing M2 myeloid cells. duanyu18136 may be a new therapeutic target for the prevention and treatment of lung cancer.

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