Fig. 5

AKR1C1 controls anti-cell death pathways and inflammatory gene networks in HNSCC cells. a The flowchart of identifying the AKR1C1 downstream genes with 1.5-fold change cutoff compared to control vectors and their possible regulators in HNSCC cells. b The disease and biological function results from the IPA database c AKR1C1 regulates inflammation proteins, such as TNF-α and TGF-β networks, by IPA in HSC-2 (d) and Cal-27 (e) cells. D. STAT family reporter activity assays. The reporter activity was normalized by the expression level of pGL4-miniP reporters in the stable cell lines. e Phosphorylation level of ^pY705STAT3 and ^pY701STAT1 in AKR1C1-expressing Cal-27 cells. f Immunoprecipitation STAT1 and STAT3 in HSC-2 cells. g and h Cisplatin dose-response curve in Cal-27 expression with wild type STAT1 or constitutive activation form STAT1-Y701F (g) or STAT3 or STAT3-Y705F. I to k. The real-time PCR validation of microarray candidates in AKR1C1 overexpression (I, Cal-27) and knockdown (J, HSC-2; K, FaDu) cells. The gene expressions were normalized with endogenous GAPDH expression. The statistical significance was analyzed by Student’s t-test. *p < 0.05 **p < 0.01, ***p < 0.001