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. 2020 Oct 28;11(10):926. doi: 10.1038/s41419-020-03108-2

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Expressions of mTORC1 and mTORC2 in clinical HCC samples. HCC samples (n = 20) were stained using antibodies to p-mTOR(Ser²⁴⁴⁸), Rictor, Raptor, and targets downstream of mTORC1 (p-4EBP1(Thr^37/46), p-S6(Ser^240/244)) and mTORC2 (p-Akt(Ser⁴⁷³)). B ZIQ-24 inhibited PI3K/AKT/mTOR signaling pathway proteins. C ZIQ-24 inhibited the expression of substrate of mTORC1. D ZIQ-24 inhibited the lipid kinases activity of mTORC. E ZJQ-24 inhibited the endogenous kinases activity of mTORC1. HepG2 and HUH-7 cells extracts were subjected to immunoprecipitation (IP) with pre-immune (IgG) or anti-Raptor. The immunoprecipitates were incubated with dephosphorylated GST–S6K1 in the presence of the indicated concentrations of ZJQ-24 or DMSO. F The expressions of VEGF, p-AKT (Ser⁴⁷³), p-mTOR (Ser²⁴⁴⁸), Raptor, Rictor, p-4EBP-1 (Thr^37/46), and p-P70S6K (Thr³⁸⁹) were measured by immunohistochemistry with tumor tissues.