Knockdown of LINC00467 inhibits gastric cancer progression by modulating the sequestration of miR-141-3p

Background Long non-coding RNAs (lncRNAs) are key targets associated with the incidence of gastric cancer (GC). Aims In this study, the ability of LINC00467 to regulate GC progression was evaluated. Methods The expression of this lncRNA was evaluated in the GEPIA database of human cancer samples, showing LINC00467 upregulation in 60 GC patient tumor tissue samples relative to paired paracancerous control tissues. Functionally, LINC00467 promoted glycolysis in GC cells and enhanced their proliferative, migratory, and invasive activities. From a mechanistic perspective, this lncRNA was able to bind microRNA (miR)-141-3p in GC cells, and a negative correlation between miR-141-3p and LINC00467 expression was observed in GC tissue samples. Results Inhibition of miR-141-3p partially reversed the effects of LINC00467 knockdown on GC cell malignancy, and LINC00467 was further found to control the expression of the miR-141-3p target gene dihydropyriminidase-like 3 (DPYSL3) in GC cells. Furthermore, lactate accumulation from glycolysis activated the Akt signaling pathway to promote the transcriptional expression of LINC00467 in GC cells, leading to persistent glycolysis and GC cell invasion. Conclusions These findings suggest that LINC00467 controls GC progression via regulating the miR-141-3p/DPYSL3 pathway.