LINC01224 promotes the Warburg effect in gastric cancer by activating the miR-486-5p/PI3K axis.

Abstract

The Warburg effect, a common feature of solid tumors, rewires the metabolism and promotes growth, survival, proliferation, and long-term maintenance in gastric cancer (GC). We performed in vitro and in vivo studies of the pathogenesis of GC to investigate the effects and mechanism of LINC01224 in this cancer. qRT-PCR was used to measure the expression of LINC01224 or miR-486-5p in GC cells, and the expression of LINC01224 in GC tissues by FISH (Fluorescence in situ hybridization) analysis was evaluated. Bioinformatics predicted the target gene of LINC01224, Western blotting was used to measure the protein expression of genes in the PI3K/AKT/mTOR/HIF-1α axis and Warburg effect in GC cells. The function of LINC01224 in GC cells was determined using measurements of EDU assay, colony formation, apoptosis, cell migration, and cell invasion. Glucose metabolism was evaluated using a glucose uptake assay and measurements of lactate. A tumor xenograft model was used to examine the effect of LINC01224 on GC growth in vivo. We found that upregulation of LINC01224 in GC cells activated the miR-486-5p/PI3K axis and promoted aerobic glycolysis, thereby increasing cell viability, proliferation, migration, invasion and anti-apoptosis. LINC01224 downregulation had the opposite effect. LINC01224 expression promoted the in vitro and in vivo pathogenesis of GC by promoting aerobic glycolysis. LINC01224 is a promising target in the treatment of GC.