Plasma metabolomics and lipidomics reveal potential novel biomarkers in early gastric cancer: An explorative study

Abstract

Background Early identification and therapy can significantly improve the outcome for gastric cancer. However, there is still no perfect biomarker available for the detection of early gastric cancer. This study aimed to investigate the alterations in the plasma metabolites of early gastric cancer using metabolomics and lipidomics based on high-performance liquid chromatography-mass spectrometry (HPLC-MS), which detected potential biomarkers that could be used for clinical diagnosis. Methods To investigate the changes in metabolomics and lipidomics, a total of 30 plasma samples were collected, consisting of 15 patients with early gastric cancer and 15 healthy controls. Extensive HPLC-MS-based untargeted metabolomic and lipidomic investigations were conducted. Differential metabolites and metabolic pathways were uncovered through the utilization of statistical analysis and bioinformatics analysis. Candidate biomarker screening was performed using support vector machine-based multivariate receiver operating characteristic analysis. Results A disturbance was observed in a combined total of 19 metabolites and 67 lipids of the early gastric cancer patients. The analysis of KEGG pathways showed that the early gastric cancer patients experienced disruptions in the arginine biosynthesis pathway, the pathway for alanine, aspartate, and glutamate metabolism, as well as the pathway for glyoxylate and dicarboxylate metabolism. Plasma metabolomics and lipidomics have identified multiple biomarker panels that can effectively differentiate early gastric cancer patients from healthy controls, exhibiting an area under the curve exceeding 0.9. Conclusion These metabolites and lipids could potentially serve as biomarkers for the screening of early gastric cancer, thereby optimizing the strategy for the detection of early gastric cancer. The disrupted pathways implicated in early gastric cancer provide new clues for additional understanding of gastric cancer's pathogenesis. Nonetheless, large-scale clinical data are required to prove our findings.