Fig. 7
A Immunoblot analysis of the indicated proteins in the pathway of the SMYD3-mediated H3K4me3high status in primary human nasal epithelial cells induced by IL-4 (T) treatment compared with controls (C) (n = 3). B Effects of IL-4 and/or BCI-121 on the SAM level in nasal epithelial cells (n = 8 per group; error bars, s.d.) and SAH levels and SAM/SAH ratios in nasal epithelial cells (group n = 6 per group; error bars, s.d) (In the SAH experiment, two of the 8 samples were completely exhausted). C Quantitative RT‒PCR analysis of the MAT2A transcript level in human nasal epithelial cells stimulated with IL-4 for the indicated times (n = 4). D Positive correlation between the mRNA expression level of MAT2A and the level of SAM (n = 10), R.2 = 0.7770. E Quantitative RT‒PCR analysis of the c-Myc transcript level in human nasal epithelial cells stimulated with IL-4 for the indicated times (n = 4). F Immunoblot analysis of the effect of MAT2A expression on primary human nasal epithelial cells pretreated with IL-4 after exposure to the c-Myc inhibitor KJ Pyr 9 (10 μM). G-H Immunoblot analysis of H3K4me3, SMYD3 and IGF2 protein expression in primary human nasal epithelial cells pretreated with IL-4 after exposure to KJ Pyr 9 (10 μM) with or without PF-9366 (10 μM). I Immunoblot analysis of c-Myc and MAT2A protein expression in primary human nasal epithelial cells pretreated with IL-4 after exposure to KJ Pyr 9 (10 μM) with or without PF-9366 (10 μM). J ELISA of IGF2 as described in (H) (n = 4). K Quantitative RT‒PCR analysis of the IGF2 transcript level as described in (H) (n = 4). Statistical significance (C and E), unpaired Wilcoxon test; (B and K), one-way ANOVA;***p < 0.001;**p < 0.01; ∗ p < 0.05