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. 2023 Jun 7;14:1207496. doi: 10.3389/fphar.2023.1207496

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Copyright © 2023 Guo, Hu, Yao and Han.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Part of potential pathways to reverse sorafenib resistance by inducing ferroptosis. Sorafenib has synergistic effects with sulfasalazine in that they both induce AMPK phosphorylation of T172, reduce the expression of transcription factor SREBP1, block BCAT2 transcription in the nucleus, reduce intracellular Glu synthesis, and decrease the xCT system activity. NHE inhibitors like amiloride can inhibit macropinocytosis, block the extra acquisition of cysteine by HCC cells, reduce intracellular cysteine levels, and increase lipid peroxidation production. In addition, metformin also modulates the p62-Keap1-NRF2 pathway and decreases HO-1 expression, thereby regulating the ROS response and inducing more ferroptosis in HCC cells.