Fig. 2

Suppression of AKR1B10 attenuated PEM-chemoresistance of BM cells in vitro and in vivo. A Western blotting showing the AKR1B10 knockdown efficiencies in PC9-BrM3 cells. B Indicated AKR1B10 knockdown PC9-BrM3 cells were treated with different doses of PEM for 72 h and CCK-8 assays were performed to determine their viability. C Results of clonogenic assays showing cell survival of the AKR1B10 knockdown PC9-BrM3 cells after treatment with certain concentrations of PEM (0, 20, 40 nM). Pixel density quantification of clonogenic assays is shown as histogram. D Flow cytometry analysis of AKR1B10 knockdown PC9-BrM3 cells treated with PEM (20 nM) for 24 h. E Heat map image representations of bioluminescence intensity for representative mice from the indicated groups of the therapy response experiment. Nude mice were implanted with PC9-BrM3 cells with or without AKR1B10 knockdown (10⁵ cells/mouse) by intracranial injection. PEM Treatments (n = 3, 100 mg/kg, once a week, i.p.) were initiated at the 3th week. Bioluminescence intensity in the same bioluminescence heat map range was measured every week. Plot of mean bioluminescence readings for control and treatment group mice; the standard error is indicated for each imaging point. (n = 3, **p < 0.01, **p < 0.0001, Ctrl, control PC9-BrM3 cells; shNC, PC9-BrM3 cells transfected with negative control shRNA; sh1, PC9-BrM3 cells transfected with AKR1B10-targeted shRNA vector 1; sh2, PC9-BrM3 cells transfected with AKR1B10-targeted shRNA vector 2; shAKR1B10, PC9-BrM3 cells transfected with AKR1B10-targeted shRNA vector 1)