Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis

Ferroptosis is a unique variety of non-apoptotic cell death, driven by massive lipid oxidation in an iron-dependent manner. Since ferroptosis was introduced as concept 2012, it has demonstrated its essential role the pathogenesis neurodegenerative diseases and important therapy-resistant cancer cells. Thus, detailed molecular understanding both canonical alternative pathways required. There set widely used chemical agents to modulate using different pathway targets: erastin blocks cystine–glutamate antiporter, system xc-; ML210 directly inactivates GPX4; L-buthionine sulfoximine (BSO) inhibits γ-glutamylcysteine synthetase, enzyme for glutathione synthesis de novo. Most studies have focused on lipidomic profiling model systems undergoing death ferroptotic modality. In this study, we developed high-quality shotgun proteome sequencing during induction three (erastin, ML210, BSO) before after 24 48 h treatment. Chromato-mass spectra were registered DDA mode are suitable further label-free quantification. Both processed raw files publicly available could be valuable dynamic map investigation.