Research Paper Volume 13, Issue 10 pp 13515—13534

Suppressing the KIF20A/NUAK1/Nrf2/GPX4 signaling pathway induces ferroptosis and enhances the sensitivity of colorectal cancer to oxaliplatin

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 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 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 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 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

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).