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. 2020 Apr 20;11(4):248. doi: 10.1038/s41419-020-2471-7

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© The Author(s) 2020

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 Two bioinformatic prediction tools, humanTFDB and JASPAR, were used to find the transcription factors that could modulate Bim expression. b Bim mRNA expression in HCC tissues was significantly correlated with FoxO3a in TCGA datasets. c The expression levels of FoxO3a and p-FoxO3a were analyzed by western blots. SPR knockdown promoted the nuclear translocation of FoxO3a in HCC cells by separation of the cytoplasm and nucleus, as revealed by the d immunofluorescence assay and e western blots. Scale bar: 20 μm. f The knockout efficiency of CRISPR/Cas9 for FoxO3a was determined by qPCR. g FoxO3a suppression abolished the upregulation of Bim expression in SPR-depleted HCC cells. h Gene silencing of FoxO3a rescued the apoptosis induced by SPR depletion in HCC cells. Data are represented as the mean ± SD of three independent experiments. The p-values < 0.05 were considered statistically significant for all tests. NC negative control.