Skip to main content
. 2014 Jul 15;5(16):6923–6935. doi: 10.18632/oncotarget.2222

Figure 6. JAK/STAT inhibitors abrogated IFNγ-induced DNA demethylation of the APM gene promoters in TC-1/A9 cells.

Figure 6

Inhibitor of Janus kinases (JAK inhibitor 1), as well as STAT1 phosphorylation inhibitor fludarabine, blocked the IFNγ induction of the MHC class I cell-surface expression (A), as well as APM gene activation (B), and caused impaired demethylation of the corresponding gene promoter regions (C). Both inhibitors blocked IFNγ-induced STAT1 phosphorylation (D). The effect of fludarabine was much weaker, as compared to Janus kinase inhibitor 1. * denotes significant changes (P<0.05 determined in Student's t-test) as compared to the values from untreated control cells. ** denotes significant changes (P<0.05 determined in Student's t-test) as compared to the values from TC-1/A9 cells after IFNγ treatment. Biological triplicates were used for the analysis. In all experiments, error bars show standard deviations. Relative expression numbers represent the percentage of the β-actin expression levels. The levels of relative gene expression were presented as fold changes compared to the levels found in control samples. U = unmethylated primer, M = methylated primer. Experiments with JAK inhibitor 1 and fludarabine were repeated five and two times, respectively, with similar results.