Fig. 7

The JAK inhibitor ruxolitinib inhibits AKR1C1-induced cisplatin-resistance and JAK-STAT signaling pathway activation. a immunoblotting of phosphorylation ^pY701STAT1 and ^pY705STAT3 status under ruxolitinib-treated Cal-27 AKR1C1 cells (2–0.5 μM). b and c The caspase 3/7 activity assay in Cal-27-AKR1C1 (b) and HSC-2 (c) cells. The cisplatin concentration is 5 μM in Cal-27 cells and 10 μM in HSC-2 cells. The ruxolitinib is treated 0.5 μM in both cells. d and e The real-time PCR results of STAT3 downstream gene expression in Cal-27-AKR1C1 (d) and HSC-2 (e) cells. f The hypothetical model of the AKR1C1 contribution to cisplatin-resistance through STAT1 and 3 activation in HNSCC. The gene expressions were normalized with endogenous GAPDH expression. The statistical significance was analyzed by Student’s t-test. n.d: non-detected, *p < 0.05 **p < 0.01, ***p < 0.001