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. 2022 Feb 23;13(2):174. doi: 10.1038/s41419-022-04624-z

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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. 5 — A Volcano plot of all expressed genes is shown to identify DEGs obtained from microarray study (GSE180601) in Selinexor-treated SK-N-BE(2) cells with abs(log₂(fold change)) >1 and adjusted p value <0.05. B KEGG pathway analysis for DEGs. C CCK-8 assays for SK-N-BE(2) cells treated with the indicated concentrations of Selinexor for 72 h. D Immunofluorescence confocal images showing the subcellular distribution of E2F7 in SK-N-BE(2) cells treated with 0.4 μM Selinexor for 24 h. E CCK-8 assays for SK-N-BE(2) cells treated with the indicated concentrations of GSK-J4 for 72 h. F CCK-8 assays for SK-N-BE(2) cells treated with 0 or 0.5 μM GSK-J4 and the indicated concentrations of Selinexor for 72 h. G, H Flow cytometry showing the apoptosis of SK-N-BE(2) cells treated with 0.5 μM GSK-J4, 0.2 μM Selinexor, or the combination for 48 h. Unpaired two-sided t-test for analysis in H, data were shown as mean ± SD (error bars). Data were representative of three independent experiments.