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. 2022 Jan 17;41:26. doi: 10.1186/s13046-022-02245-0

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — The SFB31/DLG1 axis promoted tumor invasion via the PI3K/AKT signaling pathway. A KEGG enrichment analysis of DEGs in SF3B1 mutant vs. wild-type human prolactinoma and GH3 cells. B Phosphorylated and total AKT and GSK-3β levels in Sf3b1 WT and mutant GH3 cells transduced with or without Dlg1-FLAG cDNA. C Phosphorylated and total AKT and GSK-3β levels in GH3, 293 T, and MCF7 cells transduced with or without DLG1 siRNA