Fig. 6From: Regulation of tNOX expression through the ROS-p53-POU3F2 axis contributes to cellular responses against oxaliplatin in human colon cancer cellsa, HCT116 cells were treated with oxaliplatin or ddH2O for 24 h, and tNOX mRNA levels were determined by RT-PCR. The presented results represent three independent experiments (**p < 0.01, ***p < 0.001 for cells treated with oxaliplatin vs. controls). b, p53-wild-type cells were co-transfected with a reporter construct and a POU3F2 expression vector, and luciferase activities were determined. The presented values (mean ± SD) represent three independent experiments performed in at least triplicate (**p < 0.01 for experimental group vs. control). c, p53-wild-type cells were transfected with the POU3F2 expression vector for 24 h and then exposed to oxaliplatin for an additional 24 h. Cell lysates were separated by SDS-PAGE and analyzed by Western blotting. β-Actin was used as an internal control. Representative images are shown. The percentage of apoptotic cells was also determined by flow cytometry; the presented values (mean ± SEs) represent at least three independent experiments (***p < 0.001 for treatments vs. controls). d, p53-null cells were transfected with the shPOU3F2 knockdown vector for 24 h and then exposed to oxaliplatin for an additional 24 h. Cell lysates were separated by SDS-PAGE and analyzed by Western blotting. β-Actin was used as an internal control. Representative images are shown. The percentage of apoptotic cells was also determined by flow cytometry; the presented values (mean ± SEs) represent at least three independent experiments (*p < 0.05, **p < 0.01, ***p < 0.001 for treatments vs. controls)Back to article page