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• W3136275244 abstract "Brain metastasis is a common complication with poor prognosis in non-small cell lung cancer (NSCLC). Radiotherapy, as the main treatment, still has unsatisfactory therapeutic effects. Microglia as brain macrophage displayed M1 or M2 phenotype depending on the microenvironment. Our previous study shows macrophage migration inhibitory factor (MIF) is overexpressed in primary tissues of NSCLC brain metastasis. Studies have reported that tumors escape M1 conversion of microglia via CD74 activation through the secretion of macrophage migration inhibitory factor (MIF). The aim of this study was to explore the effects of radiosensitization by inhibiting the MIF/CD74 axis to regulate the polarization of microglia to M1 phenotype in NSCLC brain metastasis. The expression of MIF was detected in 4 NSCLC patients with brain metastasis and matched peritumoral tissues. ShRNA was applied to silence CD74 and MIF in BV2 cells and Lewis cells. M1 and M2 markers were detected by Western Blot, RT-PCR, immunofluorescence staining and flow cytometry. The phagocytosis of microspheres and Lewis cells in BV2 cells was detected by immunofluorescence staining and flow cytometry. The co-culture of Lewis and BV2 cells was constructed using transwell chambers. The wound healing and transwell assays were used to detect the migration of BV2 cells. The colony formation assay, Annexin V/7-AAD staining and PI staining were utilized to determine the effects of MIF/CD74 axis and HIF-1α/MIF on Lewis cells. In vivo model of brain metastasis was established to explore the effects of HIF-1α/MIF/CD74 signaling. The expression of MIF was significantly higher in brain tumors than peritumoral tissues, and high MIF expression indicated poor prognosis. Silencing CD74 promoted irradiated BV2 cells to M1 phenotype transformation. Co-culture of Lewis cells and irradiated BV2 cells showed that inhibition of MIF/CD74 axis promoted M1 polarization of BV2 cells, enhanced the ability of phagocytosis and migration in BV2 cells. Co-culture supernatant added to Lewis cells inhibited the proliferation and colony formation, induced apoptosis of Lewis cells. KC7F2 (HIF-1α inhibitor) inhibited MIF secretion and the binding of HIF-1α to MIF promoter in Lewis cells. Collecting the supernatant of Lewis cells with KC7F2 under hypoxic conditions, and added to irradiated BV2 cells knockdown CD74 for 24h. The results showed that inhibiting HIF-1α/MIF axis could transform BV2 cells to M1 phenotype, promoted the phagocytosis and migration of BV2 irradiated cells. Then, we collected the medium in BV2 cells, and applied to Lewis cells. We found that inhibition of HIF-1α/MIF/CD74 axis could inhibit the colony formation, remodel cell cycle distribution of Lewis cells, resulting cell apoptosis. The in vivo experiments indicated that radiation The in vivo experiments showed that inhibition of MIF/CD74 axis could improve hypoxia state of tumors and transform macrophages to M1 phenotype, leading to the shrinkage of brain tumors caused by radiotherapy, prolong survival time. Mechanically, we identified that MIF/CD74 pathway regulated phenotypic transformation of BV2 cells may by activating PI3K/AKT signaling. The HIF-1α/MIF/CD74 axis could be used as a target for radiation therapy, providing a new research basis and theoretical basis for the treatment of NSCLC brain metastases." @default.
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• W3136275244 date "2021-03-01" @default.
• W3136275244 modified "2023-10-16" @default.
• W3136275244 title "P63.03 M1 Phenotype Polarization of Microglia via MIF/CD74 Axis for Radiosensitization in NSCLC Brain Metastasis" @default.
• W3136275244 doi "https://doi.org/10.1016/j.jtho.2021.01.989" @default.
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