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
Figure 3. KIF20A induced NUAK1 activation to up-regulate GPX4 level, thus inducing CRC resistance to Oxaliplatin. (F) Cell death was assessed by LDH release assay to observe whether ETC-1002 would affect the lethal effect of oxaliplatin on KIF20A-silenced colorectal cancer cells in vitro. Top, HCT116-Or cells. Bottom, H716 cells. The data are presented as the mean ± SD, ***p < 0.001 (versus shKIF20A+Oxaliplatin). (G) The cellular LIP was analyzed with a flow cytometer to observe whether ETC-1002 would affect the LIP induction of oxaliplatin on KIF20A-silenced colorectal cancer cells. Left, HCT116-Or cells. Right, H716 cells. The data are presented as the mean ± SD, ***p < 0.001 (versus shMOCK+Oxaliplatin). (H, I) The cellular level of ROS (H) and lipid peroxidation (I) was assessed by flow cytometry to observe whether ETC-1002 would affect the oxidative damage induction of oxaliplatin on KIF20A-silenced colorectal cancer cells. Left, HCT116-Or cells. Right, H716 cells. The data are presented as the mean ± SD, ***p < 0.001 (versus shKIF20A+Oxaliplatin).