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. 2021 Nov 16;40:364. doi: 10.1186/s13046-021-02154-8

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© The Author(s) 2021, corrected publication 2022

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. 1 — Effect of drugs on cell viability, cell proliferation and FAK phosphorylation in HCC cells. Dose-response curves and IC50 fit lane for PND1886 (A), PF431396 (B), TAE226 (C), and SOR (D) in HepG2 and Huh7 cells. Values are measured by XTT assay after 48 h from treatment and expressed as percentage of killed cells respect to NT ± Standard Deviation (SD) of three independent experiments. E Proliferation rate in HCC cells after treatment with IC50 values in HepG2 and Huh7 cells. Values are expressed as percentage respect to NT cells of the mean of at least three independent experiments. F Representative immunoblot by WB of pTyr397FAK expression after 48 h from treatment with the different drugs, in HepG2 and Huh7 cells. αTubulin served as loading control