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. 2024 Jan 10;22:43. doi: 10.1186/s12967-023-04830-z

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© The Author(s) 2024

Open Access This 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. 7 — Model depicting the anti-HCC actions of PF-543. Elevated pro-angiogenic factors, exemplified by VEGF-A, act through their receptors to drive sprouting angiogenesis in tumor endothelial cells (EC), promoting tumor neovascularization and HCC progression. PFKFB3 serves as a molecular switch in this process, dictating the glycolytic energy supply that is essential for sprouting angiogenesis. The selective SphK1 inhibitor PF-543 abrogates S1P production, subsequently turning off the PFKFB3-mediated glycolytic switch, which leads to the inhibition of sprouting angiogenesis and eventually suppression of HCC progression. The graphical abstract was created with BioRender.com. . The 3D conformer of PF-543 was adapted from PubChem, pubchem.ncbi.nlm.nih.gov, CID 66,577,038