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. 2022 Jun 2;29:34. doi: 10.1186/s12929-022-00817-y

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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. 4 — The TGF-β and JAK/STAT3 pathways are highly enriched in HCC clinical samples with increased DYRK1A expression. a and b Data collected from the LinkedOmics platform (www.linkedomics.org/admin.php) are shown. Sample cohort: The Cancer Genome Atlas_liver HCC; Institute: UNC; Data type: RNAseq; Platform: HiSeq RNA; Attribute: DYRK1A; Statistical methods: Pearson correlation test; Patients: 371; Tool: GSEA, Enrichment Categories: a PANTHER pathways and b WikiPathways. c The TGF-β, JAK/STAT3 and EGF/EGFR signalling pathways were enriched in the DYRK1A high expression group in both the WikiPathways and PANTHER pathways analyses. d and e GSEA was performed, and the results indicated that DYRK1A could play an important role in regulating the TGF-β and JAK/STAT3 pathways