Fig. 3
From: SWI/SNF catalytic subunits’ switch drives resistance to EZH2 inhibitors in ARID1A-mutated cells
SMARCA4 loss promotes resistance to EZH2 inhibitors by upregulating an anti-apoptosis gene signature. a ChIP-seq profiles of SMARCA4 in parental and resistant cells. TSS: transcription starting sites. b ChIP-seq tracks of SMARCA4 on its own promoter region in endogenously FLAG-tagged parental and resistant cells. Arrow points to the loss of SMARCA4 binding in its own promoter region. c ChIP-qPCR validation of a decrease of SMARCA4 binding to its own promoter. d Venn diagram showing the genome-wide overlap analysis between SMARCA4 ChIP-seq and genes upregulated in RNA-seq in parental and resistant cells. e Top pathways enriched among the genes identified in d. f ChIP-seq tracks of SMARCA4 on the BCL2 promoter region in endogenously FLAG-tagged parental and resistant cells. g, h qRT-PCR (g) and immunoblot (h) of BCL2 levels in parental and resistant cells. i, j ChIP-qPCR validation of a decrease in SMARCA4 binding on the BCL2 promoter in resistant cells using antibodies against endogenously tagged FLAG (i) or endogenous SMARCA4 (j). Data represent mean ± S.E.M. of three independent experiments (c, g–j). P-value was calculated via two-tailed t-test
