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. 2021 Nov 23;12:785463. doi: 10.3389/fimmu.2021.785463

Figure 3.

Figure 3

HOTAIR may regulate gene expression pattern in an NF-κB-dependent manner in glioma. (A) The enrichment plots of gene expression signatures of HOTAIR-induced IL6-JAK-STAT3 signaling and TNFα signaling via NF-κB, and the signatures of samples annotated in mesenchymal glioma and proneural glioma, sorted according to the differences between the samples with high and low level HOTAIR expression. (B) Enrichment heatmap showed the NFκB-dependent biological processes associated with the grade of samples. (C, D) NF-κB regulated gene expression levels in U87 (C) and TBD (D) at 24 hours after treatment with AQB. Values are means ± s.d. from n = 3 independent experiments. The P value was determined by two-sided Student’s t-test. (E) Immunobolts detect the protein level of NF-κB and pNF-κB, using GAPDH as control in U87 cells treated with AQB at the concertration of 40μM and 80μM. (F) Immunoblots showing the effect of AQB on expression of PD-L1 and EZH2 in U87 and TBD cells, using GAPDH as control. (G) Immunoflourescence showing the protein level and protein distribution of H3K27me3, NF-κB and PD-L1 in DMSO or AQB treated U87 cells. The bar chart indicates differences in the mean optical densities of NF-κB, PD-L1, and H3K27me3 proteins in DMSO or AQB-treated U87 cells. Scale bar, 50μm. ***P < 0.001, ****P < 0.0001.