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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. 9 — DYRK1A promotes EMT and metastasis of hepatocellular carcinoma cells by cooperatively activating STAT3 and SMAD. DYRK1A interacted with TSC1 and activated SMAD2/3 and also interacted with and activated STAT3 in HCC cells. Thus, DYRK1A promoted EMT and metastasis of HCC cells by activating STAT3 and SMAD gene transcription program in an independent way