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MS-Based Metabolomics Reveals Metabolic Dysregulation in Erastin-Induced Gastric Adenocarcinoma Cells


 Gastric cancer (GC) is one of the most malignant tumors with high morbidity and mortality in the world, particularly in China. Erastin, a classical ferroptosis inducer, exerts cytotoxicity in several types of cancer cells including gastric cancer cells. However, the mechanism of erastin in regulating metabolic pathways in gastric cancer remains largely unclear. To investigate the gastric cellular response to erastin therapy, we adopted a cell pseudotargeted metabolomics method based on liquid chromatography-hybrid triple quadrupole linear ion trap mass spectrometry (LC-QTRAP MS). The developed method was used to investigate the differential metabolites between erastin-treated MGC-803 cells and the controls at different time points. We found that erastin induced tremendous impact on the metabolome of gastric cells by affecting key metabolic processes, such as cysteine and methionine metabolism, glutathione (GSH) biosynthesis, glycolysis and TCA cycle. Interestingly, S-adenosylmethionine (SAM), methionine, serine, glycine and cysteine were obviously increasing treads after erastin treatment, but S-adenosylhomocysteine (SAH) and GSH were always down-regulated up to 48 h. The results indicated that DNA methylation was activated and glutathione biosynthesis was blocked in erastin-treated MGC-803 gastric cells, highlighting the importance of erastin as a promising drug candidate for in vivo treatment of gastric tumor.