Fig. 4: HDAC2 knockout decreased IFNγ-induced STAT1 recruitment and histone acetylation of PD-L1 promoter. | Cell Death & Disease

Fig. 4: HDAC2 knockout decreased IFNγ-induced STAT1 recruitment and histone acetylation of PD-L1 promoter.

From: Histone deacetylase 2 knockout suppresses immune escape of triple-negative breast cancer cells via downregulating PD-L1 expression

Fig. 4

A ChIP-qPCR was performed after 4T-1 cells (WT, HDAC2-KO) were treated with or without IFNγ (100 U/ml) for six hours (n = 3). B 4T-1 (WT, HDAC2-KO) cells were cultured with IFNγ (100 U/ml) for 24 h, and western blotting was performed after cells were precipitated with antibodies of HDAC2 or IgG. C, D The sequence (C) and position (D) of the binding sites of STAT1 in PD-L1 promoter. E–H ChIP-qPCR was performed using STAT1 (E), BRD4 (F), H3K27ac (G), and H3K9ac (H) antibodies after 4T-1 cells (WT, HDAC2-KO) were treated with or without IFNγ (100 U/ml) for six hours (n = 3). I Western blotting was conducted after 4T-1 (WT, HDAC2-KO) cells were stimulated with or without IFNγ (100 U/ml) for 12 h.

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