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. 2020 Aug 18;39:163. doi: 10.1186/s13046-020-01669-w

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© The Author(s) 2020

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. 2 — Regulation of ASPH expression and ASPH involvement in signaling pathways. The expression of the ASPH protein can be regulated at several levels. The ASPH gene can be amplified in tumor cells and its transcription activated by IN/IGF-1 and Wnt/ β-catenin pathways or induced by hypoxia. At the posttranscriptional level, miR-200a and miR-135a can downregulate ASPH expression. Stability of the ASPH protein can be reduced by phosphorylation with GSK-3β. Conversely, ASPH can enhance GSK-3β activity by inhibition of its phosphorylation with AKT and p38 kinases. ASPH also supports cell proliferation, epithelial-mesenchymal transition, migration, invasion, and angiogenesis and consequently tumor growth and metastasis by hydroxylation of the Notch receptor and ligands (ex. JAG) and interaction with pRb, vimentin and ADAMs. Finally, inactivation of NK cells by ASPH has been demonstrated. Green arrow, activation signal; red bar, inhibitory signal