Fig. 6.

Cigarette metabolites control AKR1C1 expression. a to c AKR1C1 promoter activity assay (a), protein (b) and mRNA level (c) in Cal-27 cells exposed to tobacco-specific nitrosamines (TSNA), such as NAB, NAT, NNK and NNN and vehicle at concentration (10 μM) for 24 h. d The phosphorylation status of ^pY701STAT1 and ^Py705STAT3 in Cal-27 cells exposed to TSNA. e The AKR1C1 induced STAT1 and 3 downstream gene expression in Cal-27 exposed to TSNA. The gene expressions were normalized by endogenous GAPDH expression. f Cisplatin dose-response curve after knockdown of AKR1C1 and co-treat with NNK or NNN. The statistical significance was analyzed by Student’s t-test. *p < 0.05 **p < 0.01, ***p < 0.001