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

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Figure 1.

Inducing ferroptosis enhanced the sensitivity of CRC to Oxaliplatin. (E) Cell (HCT116-Or) death was assessed by flow cytometry (annexin V-FITC/PI staining) to observe whether RSL3 with or without the indicated inhibitors 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 Oxaliplatin). (F) Cell (HCT116-Or) death was assessed by LDH release assay to observe whether RSL3 with or without the indicated inhibitors would affect the lethal effect of oxaliplatin on colorectal cancer in vitro. The data are presented as the mean ± SD, ***p < 0.001 (versus Oxaliplatin). (G) The cellular LIP was analyzed with a flow cytometer to observe whether RSL3 with or without liproxstatin-1 (or deferoxamine) would affect the LIP induction of oxaliplatin on colorectal cancer cells. Left, HCT116-Or cells. Right, H716 cells. The data are presented as the mean ± SD, ***p < 0.001 (versus oxaliplatin). (H, I) The cellular level of ROS (H) and lipid peroxidation (I) was assessed by flow cytometry to observe whether RSL3 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 Oxaliplatin).