Skip to main content
. 2018 Jan 23;13(1):e0191607. doi: 10.1371/journal.pone.0191607

Fig 4. SOD1 gain-of-function and NAC exposure counteract miR-143-induced oxidative stress in HCT116 human colon cancer cells.

Fig 4

HCT116 cells stably transduced with miR-143, miR-145, or Empty vector were transfected with pCI-neo (pCI) or pCI-neo-SOD1 (pCI-SOD1) plasmids, or exposed to NAC and treated with oxaliplatin (Ox). (a) SOD1 steady-state levels were analysed by immunoblotting. (b) ROS levels were determined by DCFH staining in SOD1 overexpressing cells. (c) ROS levels were determined by DCFH staining in cells treated with oxaliplatin (Ox) overexpressing SOD1 (top) or exposed to NAC (bottom). Representative blots are shown. Results are expressed as mean ± SEM fold change to Empty control cells, from at least three independent experiments. #p < 0.05 from Empty cells transfected with pCI-neo construct; †p < 0.01 from respective pCI-neo transfected cells; §p < 0.05 and ‡p < 0.01 from Empty cells treated with oxaliplatin; **p < 0.01 and ***p < 0.001 from respective oxaliplatin treated cells.