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. 2023 Aug 26;21:575. doi: 10.1186/s12967-023-04432-9

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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/. 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. 8 — GPX3 antagonized autophagy-related ferroptosis and activated ERK1/2 with the involvement of AMPK A Relative densitometric quantification of proteins (AMPK, p-AMPK, mTOR and p-mTOR) in BPH-1 and WPMY-1 cells treated with RSL3 (0.5 μM) or GPX3 plasmid, and GPX3 overexpression reversed the up-regulation of p-AMPK and down-regulation of p-mTOR caused by RSL3 treatment. B Relative densitometric quantification of proteins (LC3B and Beclin1) in BPH-1 and WPMY-1 cells treated with GPX3 plasmid or GSK621 (20 μM), and GPX3 overexpression reversed the up-regulation of autophagy caused by GSK621 treatment. The content of iron (C), MDA (D) and GSH (E) in BPH-1 and WPMY-1 cells treated with GPX3 plasmid or GSK621 (20 μM) were detected by colorimetric assay kit. F DCFH-DA fluorescent probe was used to analyze the accumulation of ROS in BPH-1 and WPMY-1 cells treated with GPX3 plasmid or GSK621 (20 μM). G Statistical analysis of mean fluorescence intensity (MFI) of DCFH-DA. The results indicated that GPX3 overexpression reversed the up-regulation of autophagy-related ferroptosis caused by GSK621 treatment. H Immunoblot assay (i) and relative densitometric quantification (ii) of ERK1/2 and p-ERK1/2 in BPH-1 and WPMY-1 cells treated with 20 μM GSK621 or GPX3 plasmid showed that GPX3 regulated ERK1/2 signaling with the involvement of AMPK pathway. GAPDH is used as loading control. ^*p < 0.05, ^**p < 0.01, ^***p < 0.001