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. 2021 Feb 24;20:38. doi: 10.1186/s12943-021-01325-7

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© The Author(s) 2021

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 — DDX3X and metastasis. a In colorectal cancer, DDX3X increases the expression of KRAS by promoting SP1 binding to the KRAS promoter. In CRC harbouring mutant KRAS, DDX3X activates the KRAS/ERK/PTEN/AKT cascade to stabilize β-catenin, which then enhances ZEB1 transcription to promote metastasis. In addition, DDX3X binds with and activates CK1ε, which then phosphorylates Dvl2. Phosphorylated Dvl2 causes dissociation of PP2A and the β-catenin degradation complex, therefore stabilizing β-catenin. The accumulated β-catenin translocates into the nucleus and interacts with TCF4 to increase the expression of its downstream target genes. b In CRC harbouring wild-type KRAS, DDX3X/KRAS/HIF1-α generates a cascade feedback loop. HIF-1α binds to the YAP1 promoter to promote YAP1 transcription. YAP1 then targets PTEN by elevating miR-29c expression to activate PI3K/AKT signalling. Phosphorylated AKT activates c-fos and eventually leads to increased levels of SIX2 transcription