Fig. 7
From: The dual role of p62 in ferroptosis of glioblastoma according to p53 status
Depletion of p62 promotes ferroptosis in p53 wild-type GBM with an intracranial xenograft model. A The CRISPR/CAS9 system was applied to construct stable p62 knockout U87 cells (CRISPR-p62-1 and CRISPR-p62-2). Knockout efficacy was verified by western blot analysis. B Representative images of pLenti-CRISPR-V2 (CTRL) (n = 8) and pLenti-CRISPR-p62-1 (CRISPR-p62) (n = 10) cells from mouse brains. C H&E and IHC analyses of p62 and SLC7A11 in orthotopic tumour sections. D Mouse survival is shown by Kaplan–Meier curves. U87-CRISPR-V2 groups, n = 8. U87-CRISPR-P62 groups, n = 10. P values were calculated using the log-rank test. E Mechanistic model for dual role of p62 in ferroptosis according to p53 status in GBM