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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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Targeting xCT rebalances lipid ROS generation during glioma ferroptosis. Fluorescence activated cell sorting-based analysis for cellular lipid ROS following 0.1 μm RSL3 application. Lipid ROS was monitored via C11-BODIPY staining. A higher C11-BODIPY positive population was observed in Nrf2 KD cells (8.81%) compared with Nrf2 OE cells (5.38%). Note, Nrf2 KD cells expressing enforced xCT showed decreased C11-BODIPY positive population (5.29%). In addition, when 400 μm sulfasalazine (SAS) applied together with 0.1 μm RSL3 in Nrf2 OE cells, C11-BODIPY positive population dramatically increased (31.14%) compare to the solely RSL3-treated group (5.38%). Oval circles indicate C11-BODIPY-positive cell population.