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. 2017 Aug 9;16(10):1864–1888. doi: 10.1074/mcp.M116.064451

Fig. 7.

Fig. 7.

Chemical inhibition of EP300 suppresses SOX2 activity in tracheobronchial basal cells. Primary tracheobronchial basal cells were infected with control vector or Lenti-SOX2 ± co-treatment with 12.5 μm CBP30 (EP300 inhibitor) or DMSO (inhibitor control). Media and inhibitor were replaced every other day, and after 5 days, gene expression quantified by qRT-PCR. Data are normalized to TBP expression and plotted as fold induction relative to vector control. Means ± S.E. of 3 replicates are shown. Significance of potential gene expression induction by SOX2 was calculated by comparing values between vector and Lenti-SOX2/DMSO using paired 2-tailed t tests. *p = 0.006 (TMPRSS11B), 0.05 (SPRR3), 0.04 (ADH7), 0.01 (KIAA1199), 0.01 (FOXE1), 0.02 (EDN1). ns = not significant. ns, p = 0.16 (PIK3CA), 0.33 (SMARCA4). Significance of potential inhibition of SOX2 activity was calculated by comparing values between Lenti-SOX2/DMSO and Lenti-SOX2/CBP30 using 2-tailed t tests. *p = 0.01 (SPRR3), 0.01 (ADH7); **p = 0.001 (KIAA1199), 0.003 (FOXE1), 0.002 (EDN1); ***p = 0.0001 (TMPRSS11B); ns, p = 0.28 (PIK3CA), 0.53 (SMARCA4).