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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: AKR1C1 controls cisplatin-resistance in head and neck squamous cell carcinoma through cross-talk with the STAT1/3 signaling pathway

Fig. 3

Ectopic AKR1C1 can promote cisplatin-resistance, anti-apoptosis response and cancer stemness in HNSCC cells. a to d The in vitro cell viability assay after combining cisplatin and ectopic AKR1C1 lentiviral particles. a and c AKR1C1 protein (left) and mRNA (right) expression after enforced expression of AKR1C1. b and d Dose-response curve after enforced expression of AKR1C1. e and f The Cal-27 in vivo cisplatin response assay in which cells were infected with or without AKR1C1 overexpression clones. e The cisplatin regimen (upper) and in vivo tumor burden (bottom, n = 5). The cisplatin was given 2 mg /kg through intraperitoneal injection (i.p.). f The tumor image and tumor weights from (e) and the scale bar indicates 1 cm length. g The cisplatin-induced caspase 3/7 activity assay with or without AKR1C1 expression. h The cancer spheroid formation assays with or without AKR1C1 expression in Cal-27 cells. The left panels indicate spheroid numbers which were calculated by ImageXpress XLS High-content system and the middle panels indicate the representative spheroid image in high magnification. The statistical significance was analyzed by Student’s t-test. **p < 0.01, ***p < 0.001

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