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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Mol Cancer Res. 2021 Mar 11;19(6):1005–1014. doi: 10.1158/1541-7786.MCR-20-0534

Figure 4. SKP2 is essential for the YAP-enhanced ferroptosis and lipid peroxidation.

Figure 4.

(A) The overexpression of YAP S127A in RCC4 cells upregulated SKP2 protein as determined by western blots.

(B) Genetic interaction between YAP and SKP2. RCC4 cells were treated with siSKP2 after YAP was stably overexpressed. The data of cell viability determined by CellTiter-Glo were normalized to the DMSO controls. n=3; mean± SEM, two-way ANOVA; n.s.: not significant; ****p < 0.0001.

(C) Inhibition of YAP or SKP2 decreases the elevated lipid peroxidation induced by erastin treatment. Representative data from one of three independent experiments in MDA-MB-231 cells are shown.

(D) The increase in lipid peroxidation triggered by YAP-S127A upon erastin treatment was abolished by SKP2 knockdown. Representative data from one of three independent experiments in RCC4 cells are shown.

(E) Overexpression of SKP2 cDNA abolished the ferroptosis resistance triggered by YAP knockdown in RCC4 cells. n=3; mean ± SEM; two-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001.