Research Paper Volume 13, Issue 10 pp 13515—13534

Figure 3. KIF20A induced NUAK1 activation to up-regulate GPX4 level, thus inducing CRC resistance to Oxaliplatin. (A) The protein-protein interaction between KIF20A and NUAK1 was screened out by String database. (B) WB assay was used to observe whether KIF20A silencing could impact the phosphorylation level of MYPT1^S445. Left, HCT116-Or cells. Right, H716 cells. (C, D) The cell (HCT116-Or (C) and H716 (D)) viability was measured to observe whether ETC-1002 would affect the suppression of oxaliplatin on KIF20A-silenced colorectal cancer cells in vitro. The data are presented as the mean ± SD, ***p < 0.001 (versus shKIF20A+Oxaliplatin). (E) Cell death was assessed by flow cytometry (annexin V-FITC/PI staining) to observe whether ETC-1002 would affect the lethal effect of oxaliplatin on KIF20A-silenced colorectal cancer cells in vitro. Left, representative results of annexin V-FITC/PI staining. Right, quantitative analysis. Top, HCT116-Or cells. Bottom, H716 cells. The data are presented as the mean ± SD, ***p < 0.001 (versus shKIF20A+Oxaliplatin).