[Abstract] Objective: To study the role of ACLY in regulating lipid metabolism during the occurrence and development of gastric cancer through bibliometric and bioinformatics analyses. Methods: The PubMed database was used to search the literature related to gastric cancer and lipid metabolism, and VOSviewer and Bibliometrix were used for analysis. The gastric cancer data were downloaded from the TCGA database, and the R software (4.2.1) and related R packages were used for data processing. The expression levels of ACLY in gastric cancer tissues and normal tissues in the TCGA database were compared. Cox regression analysis was used to explore the risk factors for and prognosis of patients with gastric cancer. ROC curves, time-dependent ROC curves, K-M survival curves and coexpression heatmaps were used to analyze the relationships between ACLY and the prognosis of patients with gastric cancer. GO and KEGG enrichment analyses of the ACLY-related genes were performed. The GeneCards database was used to screen and analyze the gene data related to ACLY-related genes, lipid metabolism and gastric cancer. The substances in HGC-27 cells treated with 2-furoic acid and normal HGC-27 cells were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Results: The prognosis of patients with lipid metabolism and development is a hot topic in the field of gastric cancer. Compared with that in normal tissues, the level of ACLY in gastric cancer tissues is significantly greater, and it is associated with poor patient prognosis. The prognosis of patients with gastric cancer is related to age, N stage and M stage. The functions of the genes related to ACLY in cell differentiation and the structure, signal transduction and enzyme activity of gastric cancer are enriched. The common differentially expressed genes related to gastric cancer, lipid metabolism and ACLY are related to ACLY. The content of fatty acids in gastric cancer cells decreased after 2-furoic acid treatment. Conclusions: ACLY regulates lipid metabolism to affect the occurrence and development of gastric cancer.