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. 2021 Jul 13;12(7):698. doi: 10.1038/s41419-021-03998-w

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a Immunoblots of xCT in wild-type (WT), SLC7A11 knockout (SLC7A11^KO), and SLC7A11 overexpressing (SLC7A11^OE) HT1080 cells. Valosin-containing protein (VCP) was used as a loading control. b Cystine uptake activity of WT and SLC7A11^OE HT1080 cells in the presence of either 10 µM erastin or sorafenib. Data are presented as mean ± s.d. (n = 4). c Cell viability of WT, SLC7A11^KO, and SLC7A11^OE HT1080 cells treated with indicated concentrations of sorafenib, sulfasalazine, or erastin, in the absence or presence of 50 μM β-mercaptoethanol (β-ME), 1 μM Lip-1, or 100 μM DFP for 24 h. Data are presented as mean ± s.d. of n = 3 wells of a 96-well plate from one representative of three independent experiments.