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. 2022 Feb 25;12:20. doi: 10.1186/s13578-022-00764-z

Fig. 5.

Fig. 5

P53 mutation status is responsible for the dual regulation of p62 on GBM ferroptosis. A Cells were transfected with pcDNA3.1 or HA-P62 plasmids, followed by DMSO, erastin or erastin + APR-246 treatment. Cell death were determined by trypan blue staining. B The levels of MDA were measured in U251 cells, which were transfected with pcDNA3.1 or HA-P62 plasmids, followed by erastin or erastin + APR-246 treatment. C The levels of GSH were measured in U251 cells, which were transfected with pcDNA3.1 or HA-P62 plasmids, followed by erastin or erastin + APR-246 treatment. D U118 cells were transfected with pcDNA3.1 or HA-P62 plasmids, followed by DMSO or erastin or erastin + APR-246 treatment. The protein expression of SLC7A11 and P62 were detected by western blot analysis. E A172 cells were transfected with pcDNA3.1 or HA-P62 plasmids, followed by DMSO or erastin or erastin + PFT-a treatment. The protein expression of SLC7A11 and P62 were detected by western blot analysis. F U251 cells were transfected with pcDNA3.1 or HA-P62 plasmids, followed by DMSO or erastin or erastin + APR-246 treatment. The protein expression of SLC7A11 and P62 were detected by western blot analysis. G U251 cells were transfected with pcDNA3.1 or HA-P62 plasmids, followed by DMSO or erastin or erastin + APR-246 treatment. The mRNA expression of SLC7A11 were detected by qPCR