Skip to main content
. 2014 Oct 24;7(5):590–604. doi: 10.1016/j.tranon.2014.08.001

Figure 9.

Figure 9

Pharmacological NQO1 inhibition. Cell proliferation assays. (A) Pancreatic and colorectal carcinoma cells were treated with ES936 for 30 minutes before treatment with DMSO (control), 0.1 μM or 0.5 μM 17-AAG for 72 hours, and cell proliferation was determined. The average of at least three experiments is represented as percentage of control. Error bars are the SEM. Clonogenic assays. HT-29 cells were pretreated with 0.1 μM ES936 during 30 minutes and then treated with DMSO (control), 0.1 μM ES936 (ES936), 0.5 μM 17-AAG (17-AAG), or 0.1 μM ES936 plus 0.5 μM 17-AAG (ES936 + 17-AAG) for 4 hours. Then, cells were seeded at a very low density, allowed to grow for 14 days, fixed, stained, and visualized and colonies formed were counted. (B) Scanned images showing colonies of HT-29 cells. (C) Graphic representation of the average of three independent experiments. Error bars are the SEM. Difference between means was statistically significant (*P < .05, **P < .01, Mann-Whitney test). NQO1 activity assays. (D) NQO1 specific activity was calculated using the dicumarol-inhibitable rate of DCPIP reduction in cell extracts of HT-29 cells, treated with DMSO (control) or 0.1 μM ES936 for 4 hours. The average of at least three experiments is indicated. ND, nondetectable (< 5 nmol DCPIP/min per mg protein).