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Fig. 4 | Experimental Hematology & Oncology

Fig. 4

From: Gut fungi enhances immunosuppressive function of myeloid-derived suppressor cells by activating PKM2-dependent glycolysis to promote colorectal tumorigenesis

Fig. 4

iNOS-derived NO is required for C. tropicalis-induced glycolysis activation in MDSCs. A, B and E WT MDSCs were stimulated with heat-inactivated C. tropicalis (MOI = 1) in combination with or without specific iNOS inhibitor SMT (as indicated concentration) for 18 h. Cell lysates were analyzed by immunoblotting for the indicated proteins. C WT MDSCs were stimulated with heat-inactivated C. tropicalis (MOI = 5) in combination with or without specific iNOS inhibitor SMT (500 µM) for 24 h. Lactate secretion by MDSCs were determined by lactate assay kit. D MDSCs were stimulated with C. tropicalis (MOI = 2) in the presence or absence of specific iNOS inhibitor SMT (500 µM), then the ECAR level of these cells was measured by Agilent Seahorse XFe96 Analyzer. F and G WT MDSCs were treated with NO donor (as indicated concentration) for 12 h. Glycolytic enzymes mRNA expression were measured by q-PCR (F). Cell lysates were analyzed by immunoblotting for the indicated proteins (G). H WT MDSCs were treated with NO donor (250 µM and 500 µM) for 24 h. Lactate secretion by MDSCs were determined by lactate assay kit. I WT MDSCs were treated with NO donor (500 µM), then the ECAR level of these cells was measured by Agilent Seahorse XFe96 Analyzer. The results shown here are expressed as the mean ± SEM. Each panel is a representative experiment of at least three independent biological replicates. *p < 0.05, **p < 0.01, ***p < 0.001. The following statistical analyses were performed: unpaired Student’s t-test or one-way ANOVA where appropriate

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