Fig. 2
Silencing of AKR1C1 can increase the cisplatin response activity in HNSCC cells through enzyme-independent functioning. a to f The in vitro cell viability assay after combining cisplatin and shAKR1C1 lentiviral particles or enzymatic AKR1C1 inhibitor, 5-PBSA, in highly AKR1C1 expressed cells. a and d AKR1C1 protein (upper) and mRNA (bottom) expression after knockdown of AKR1C1. b and e Dose-response curve after knockdown of AKR1C1. c and f The cell viability assay under cisplatin IC50 and with or without AKR1C1 inhibitor, 5-PBSA (500 nM). g and h The HSC-2 in vivo cisplatin response assay in which cells were infected with or without AKR1C1-CDS knockdown clones. g The cisplatin regimen (upper) and in vivo tumor burden (bottom, n = 5). The cisplatin was given 2 mg/kg through intraperitoneal injection (i.p.).h The tumor image and tumor weights from (g) and the scale bar indicates 0.5 cm length. The statistical significance was analyzed by Student’s t-test. **p < 0.01, ***p < 0.001