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. 2021 May 13;23(12):2014–2027. doi: 10.1093/neuonc/noab114

Fig. 5.

Fig. 5

Silencing of MEF2C promoted ferroptosis by downregulating NF2 and E-cadherin. CH157 (A–G) and IOMM-Lee (H–P) cells were stimulated by 6 µM Erastin for 24 hours to trigger ferroptosis. (A–E) Western blot and densitometry quantification for MEF2C (B), E-cadherin (C), ACSL4 (D), and GPX4 (E). GAPDH was used as a control. (F) Lipid peroxidation tested by MDA assays. n = 3 experiments. (G) Cytotoxicity tested by LDH assays. n = 3 experiments. (H–M) Western blot and densitometry quantification for MEF2C (I), E-cadherin (J), NF2 (K), ACSL4 (L), GPX4 (M), and P-YAP (S-127) (N). GAPDH was used as a control. n = 3 experiments. (O) Lipid peroxidation tested by MDA assays. n = 3 experiments. (P) Cytotoxicity tested by LDH assays. n = 3 experiments. *P < .05, **P < .01, and ***P < .001. Error bars represent SD. Abbreviations: ACSL4, acyl-CoA synthetase long-chain family member 4; GPX4, glutathione peroxidase 4; MEF2C, myocyte enhancer factor 2C; NF2, neurofibromatosis type 2.