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. 2022 Feb 18;13(2):160. doi: 10.1038/s41419-021-04471-4

Fig. 5. KDM2A promotes Treg cell proliferation and glioma immune tolerance by upregulating JAG1 through affecting H3K4me3 in the JAG1 promoter.

Fig. 5

A JAG1 expression in glioma tissues (N = 40) and normal brain tissues (N = 10) determined by RT-qPCR. B JAG1 expression in glioma tissues (N = 40) and normal brain tissues (N = 10) detected by IHC. C Correlation analysis between KDM2A and JAG1 in glioma tissues (N = 40) using Pearson’s correlation coefficient. D KDM2A mRNA and protein expression in LN229 and A172 cells treated with si-KDM2A-1 and si-KDM2A-2 determined by RT-qPCR and Western blot analysis. E The enrichment of KDM2A and H3K4me3 on the JAG1 promoter determined by ChIP. LN229 and A172 cells were treated with si-NC + oe-NC, si-KDM2A-1 + oe-NC, or si-KDM2A-1 + oe-JAG1. F JAG1 and KDM2A mRNA and protein expression in LN229 and A172 cells determined by RT-qPCR and Western blot analysis. G LN229 and A172 cell proliferation detected by CCK-8 assay. H Ratio of CD4+CD25+Foxp3+ cells in CD4+ cells co-cultured with LN229 and A172 cells analyzed by flow cytometry. *p < 0.05. Data were shown as the mean ± standard deviation from. Statistical comparisons were performed using unpaired t-test when only two groups were compared or by one-way ANOVA with Tukey’s post hoc test when more than two groups were compared. Variables were analyzed at different time points using two-way ANOVA with Bonferroni post hoc test. Cell experiments were repeated three times.