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. 2023 Aug 23;23:789. doi: 10.1186/s12885-023-11239-w

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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. 7 — ACADM upregulated GPX4 via mevalonate pathway. (A) Gene set enrichment analysis of cholesterol metabolism-related genes in ACADM knockdown cell vs. the control group. (B) Free cholesterol level of each PC cells after ACADM knockdown of overexpression. (C) The level of MVA-signature expression was detected in sh-control and sh-ACADM cells by qPCR. (D) Cell viability of PC cells in three group (GEM + sh-Ctrl,GEM + sh-ACADM, GEM + sh-ACADM + MVA). (E) Cell viability of PC cells in three group (GEM + ad-Ctrl,GEM + ad-ACADM, GEM + ad-ACADM + Atorvastatin). (F) The GPX4 level of each PC cells were detected by WB. (G) The concentration of glutathione (GSH) was assayed