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. 2021 Jan 13;11:874. doi: 10.1038/s41598-020-79536-z

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© The Author(s) 2021

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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Determination of action mechanism of Mito-FF in relation with ROS and p53. (A) Immunofluorescent staining of p53 in Huh-S/R cells before and after sorafenib treatment. Following sorafenib treatment to Huh7-S cells, there was an increase in the percentage of cells with positive nuclear staining for p53; following sorafenib to Huh7-S cells, there was not. (B) Immunofluorescent staining of p53 in Huh-S/R cells before and after Mito-FF treatment. There was an increase in the percentage of cells with positive nuclear staining for p53following Mito-FF treatment to both Huh7-S/R cells. (C) Possible mechanism of sorafenib and Mito-FF in relation with mitochondrial ROS and p53. Sorafenib treatment decreases AKT/ERK in Huh7-S cells and thus increases the expression of p53, cumulating in increasing apoptosis. Sorafenib treatment did not increase apoptosis in Huh7-R cells—because AKT/ERK was increased in Huh7-R cells and thus p53 was decreased. Treating Mito-FF to Huh7-S/R cells, leads to a significant increase of mitochondrial ROS, by way of evoking mitochondrial dysfunction due to the accumulation and self-assembly in the mitochondrial matrix, resulting in increased expression of p53, which prompts apoptosis.