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. 2023 May 13;21:323. doi: 10.1186/s12967-023-04167-7

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© The Author(s) 2023

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. 5 — The PI3K-Akt-mTOR pathway influences TGF-β1-induced PMT by regulating HKII. A Immunofluorescence staining of HKII (green) and nuclei (blue) and quantitative data with or without inhibition of the PI3K-Akt-mTOR pathway. B Gene expression of HKII with or without inhibition of the PI3K-Akt-mTOR pathway. C HK activity with or without inhibition of the PI3K-Akt-mTOR pathway. D, E HKII rescue experiments showed that HKII overexpression rescued PMT induced by TGF-β1. F LY294002 decreased the mRNA expression of HKII. Scale bar = 50 μm. Data are presented as the mean ± SD (n = 3–8)