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. 2017 Aug 14;6(8):e371. doi: 10.1038/oncsis.2017.65

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Copyright © 2017 The Author(s)

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Nrf2-Keap1 pathway induces resistance to ferroptosis in U87 glioma cells. (a) Analysis of cell viability under erastin treatment on human glioma cell line U87. DMSO treatment served as vehicle. The O.D. value of vehicle treated cells was set to 100%. Nrf2 KD, Nrf2 DN and Keap1 OE U87 cells showed significantly more vulnerability to 10 μm erastin treatment (80%, 85% and 68% decrease, respectively, vs control’s 60% decrease in cell viability), while Nrf2 OE and Keap1 KD U87 cells were more resistant to erastin (46% and 38% decrease, respectively, vs control’s 60% decrease in cell viability). Values are given as mean±s.d. Statistical significance was tested by One-way ANOVA, *P<0.05, with n=6. (b) Ferrostatin-1 (1 μm) treatment rescued erastin-induced ferroptosis in each group of U87 cells. Normalized quantification of O.D. value indicated an increase in cell viability of each group respectively: Ctrl vector (56%), Nrf2 KD (56%), Nrf2 OE (43%), Keap1 KD (15%) and Keap1 OE (48%). Values were given as mean±s.d. Statistical significance was tested by one-way ANOVA, *P<0.05, with n=6. ANOVA, analysis of variance.