IFN-γ induces HLA-E via JAK–STAT3 signaling. (IMAGE)
Caption
(A) Principal component analysis of transcriptomes from control and IFN-γ-treated tumor cells. (B) Volcano plot of differentially expressed genes after IFN-γ stimulation. (C) Heatmap of IFN-γ-responsive genes. (D) HLA-E expression levels in control versus IFN-γ-treated cells. (E) KEGG pathway enrichment analysis. (F) Gene set enrichment analysis. (G) Western blot analysis of JAK–STAT3 pathway activation and HLA-E expression in HepG2 cells treated with IFN-γ, with or without the JAK inhibitor ruxolitinib. (H) Flow cytometric analysis of surface HLA-E expression in HepG2 cells under the same treatment conditions. (I) Western blot analysis of STAT3 silencing efficiency and its effect on HLA-E protein levels in HepG2 cells. (J) Flow cytometric assessment of HLA-E surface expression following STAT3 silencing in HepG2 cells. (K) Dual-luciferase reporter assays. (L) CUT&RUN assays.
Credit
Zhao Shu, Junfeng Guo, Lin Lv, Zhenxiang Peng, Shengtao Liao, Chuanfei Li, Zhechuan Mei
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