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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: B3GALT4 remodels the tumor microenvironment through GD2-mediated lipid raft formation and the c-met/AKT/mTOR/IRF-1 axis in neuroblastoma

Fig. 7

Treatment of lipid raft inhibitor, MβCD, suppresses low B3GALT4-mediated NB progression and CD8+ T cells recruitment. A The effects of MβCD on 9464D cell proliferation were measured by a CCK-8 assay. B The impacts of MβCD on 9464D cell migration and invasion. C Western blot and ELISA have shown that the treatment of MβCD can enhance knockdown B3GALT4-mediated CXCL9 and CXCL10 production and inhibit caveolin-1 expression in lipid rafts. D Western blot showed that the treatment of MβCD could reverse knockdown B3GALT4-mediated activation of the c-Met/AKT/mTOR pathway. E Chemotaxis assays showed that the treatment of MβCD could improve knockdown B3GALT4-mediated CD8+ T cell migration. F The in vivo experimental procedure scheme was detailed in the “Materials and Methods” and “Results” sections. G In vivo assays showed that the treatment of MβCD could block knockdown B3GALT4-mediated NB growth. H Flow cytometric analyzed the population of intratumoral CD8+ T cells between groups on day 27, respectively, n = 5. I Representative IHC images of serial sections derived from the tumor xenografts were stained for caveolin-1, CD8A, CXCL9, and CXCL10. Left, representative pictures of IHC staining (scale bar: 100 μm). Right, a statistic of CD8+ T cells per section, the digital quantification of the histoscore of CXCL9 and CXCL10

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