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. 2023 Jul 21;13:11795. doi: 10.1038/s41598-023-38596-7

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© The Author(s) 2023

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/.

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NVS-ZP7-4 inhibited PI3K/AKT pathway in HCC cells. HCCLM3 and Huh7 cells were treated with DMSO, 1 μM NVS-ZP7-4, PI3K activator 740 Y-P, or a combination of 1 μM NVS-ZP7-4 and 740 Y-P. (A,B) Western blotting analysis of p-ZIP7, ZIP7, and PI3K/AKT pathway targeted genes p-AKT, AKT in HCCLM3 and Huh7 cells after different treatment. (C,D) Apoptosis was evaluated (C) and quantified (D) by flow cytometry. (E) Cell cycle was evaluated and quantified by flow cytometry. (F) Cell proliferation was detected via CKK-8 at 0 h, 24 h, 48 h, 72 h. ns = no significance, *p < 0.05, **p < 0.01, ***p < 0.001 versus Control. #p < 0.05, ##p < 0.01; ###p < 0.001 versus the 1 μM NVS-ZP7-4.