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Glioma is the most frequent primary malignancy in the brain; temozolomide (TMZ) is the first-line chemotherapeutic agent used to combat this tumor. We showed here that astrocyte elevated gene-1 ( AEG-1 ) was overexpressed in glioma tissues and associated with a worse subtype and a poor prognosis. CCK-8 proliferation assays and clone formation experiments presented that  AEG-1  knockdown sensitizes glioma cells to TMZ. The  γH2AX  foci formation assays indicated that  AEG-1  silencing promotes TMZ-induced DNA damage in glioma cells. Glioma-associated microglia/macrophages (GAMs), the largest subpopulation infiltrating glioma, play important roles in the tumor microenvironment. Bioinformatics analyses and functional studies demonstrated that  AEG-1  silencing decreased M2-polarization of HMC3 microglia and the secretion of tumor supportive cytokines  IL-6  and  TGF-β1 . The expression of  AEG-1  was positively associated with M2 markers in glioma tissues varified by IHC staining. Based on the results of Affymetrix microarray and GSEA analyses, Western blot and Co-Immunoprecipitation assays were conducted to show that  AEG-1  activates Wnt/β-catenin signaling by directly interacting with  GSK-3β . The co-localization of  AEG-1  and  GSK-3β  in the cytoplasm of glioma cells was detected through immunofluorescence staining. This study raises the possibility that targeting  AEG-1  might improve the efficiency of chemotherapy and reduce immunosuppressive M2 GAMs in glioma.

AEG-1 silencing attenuates M2-polarization of glioma-associated microglia/macrophages and sensitizes glioma cells to temozolomide