Research Paper Volume 13, Issue 10 pp 13515—13534

Figure 2. High KIF20A expression in resistant CRC cell line suppressed the intracellular ferroptosis process. (G, H) The cell (HCT116-Or (G) and H716 (H)) viability was measured to observe whether KIF20A silencing with or without liproxstatin-1 would affect the suppression of oxaliplatin on colorectal cancer in vitro. The data are presented as the mean ± SD, ***p < 0.001 (versus shMOCK+Oxaliplatin). (I) Cell (HCT116-Or) death was assessed by flow cytometry (annexin V-FITC/PI staining) to observe whether KIF20A silencing with or without liproxstatin-1 would affect the lethal effect of oxaliplatin on colorectal cancer in vitro. Left, representative results of annexin V-FITC/PI staining. Right, quantitative analysis. The data are presented as the mean ± SD, ***p < 0.001 (versus shMOCK+Oxaliplatin). (J) Cell (HCT116-Or) death was assessed by LDH release assay to observe whether KIF20A silencing with or without liproxstatin-1 would affect the lethal effect of oxaliplatin on colorectal cancer in vitro. The data are presented as the mean ± SD, ***p < 0.001 (versus shMOCK+Oxaliplatin). (K) The cellular LIP was analyzed with a flow cytometer to observe whether KIF20A silencing with or without liproxstatin-1 would affect the LIP induction of oxaliplatin on HCT116-Or cells. The data are presented as the mean ± SD, ***p < 0.001 (versus shMOCK+Oxaliplatin). (L, M) The cellular level of ROS (L) and lipid peroxidation (M) was assessed by flow cytometry to observe whether KIF20A silencing with or without liproxstatin-1 would affect the oxidative damage induction of oxaliplatin on HCT116-Or cells. The data are presented as the mean ± SD, ***p < 0.001 (versus shMOCK+Oxaliplatin).