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. 2022 Jan 21;13(1):73. doi: 10.1038/s41419-022-04524-2

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© The Author(s) 2022

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. 1 — A The interference effect of shNKAP in U87MG and U251 cell lines. GAPDH was used as a loading control. B Protein overexpression level induced by Lv-NKAP in glioblastoma cell lines. GAPDH was used as a loading control. C The growth curves of the U87MG and U251 cells were examined using a CCK-8 assay. Cell growth was inhibited by NKAP knockdown and partially reversed by 0.5 μM ferrostatin-1 or 5 μM alpha-tocopherol for 24 h. D Live (green)/dead (red) staining revealed a higher cell death rate in the shNKAP group, which could be reversed by 0.5 μM ferrostatin-1 or 5 μM alpha-tocopherol for 24 h. Scale bar = 100 μm. E Cell death induced by NKAP knockdown in the absence or presence of 0.5 μM ferrostatin-1 or 5 μM alpha-tocopherol for 24 h detected by flow cytometry in U87MG and U251 cell lines. F LDH release induced by NKAP knockdown in the absence or presence of 0.5 μM ferrostatin-1 or 5 μM alpha-tocopherol for 24 h. All bars show the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01.