LncRNA CASC19 Regulates mTOR Pathway to Affect Aerobic Glycolysis and Promote the Proliferation of Gastric Cancer in Vitro and in Vivo

Aim This study aimed to investigate the function and mechanism of LncRNA CASC19 in gastric cancer (GC) in vitro and vivo. Method Metabolomics and bioinformatics methods were used to study the changes of metabolites and metabolic pathways in GC cells, wherein CASC19 expression was knocked down. The expression levels of phosphorylated mammalian target of rapamycin (p-mTOR) and different aerobic glycolysis related proteins were detected in cell experiments and animal experiments. After overexpression or knockdown of CASC19 in GC cells, we measured lactate levels and glucose consumption. In the nude mice experiment, the growth curve of the transplanted tumor was created, and the tumor weight difference between the two groups was finally compared. Result Various metabolites were screened after knocking down CASC19 expression in GC cells. Bioinformatics analysis showed that different metabolites were significantly enriched in the mTOR pathway. The results of in vitro and in vivo experiments showed that p-mTOR expression levels and various downstream proteins of the mTOR pathway related to aerobic glycolysis were significantly decreased after knocking down CASC19 expression in GC cells. CASC19 expression in GC cells was positively correlated with glucose uptake and lactate production. Conclusion Metabolomics and bioinformatics analyses showed that CASC19 could regulate the levels of various metabolites and was related to different metabolic pathways. CASC19 can regulate the expression of aerobic glycolysis related proteins by affecting the mTOR pathway and controls gastric cancer cell proliferation in vitro and in vivo.