Gastric cancer (GC) is one of the most common malignancies globally, with notable morbidity and mortality rates. Despite advances in surgical techniques and adjuvant therapies, recurrence and metastasis remain major challenges, highlighting the need for novel biomarkers and therapeutic targets. Long non-coding RNAs (lncRNAs) have emerged as key regulators in various types of cancer, including GC, which can influence tumor progression through diverse mechanisms. LINC00467, in particular, has been implicated in non-small cell lung cancer, hepatocellular carcinoma and colorectal cancer, but the role of LINC00467 in GC remains poorly understood. The present study aimed to elucidate the role of LINC00467 in GC progression by investigating its expression patterns, functional impact on cellular behaviors and underlying molecular mechanisms. The expression levels of LINC00467 were evaluated in the GEPIA database of human gastric cancer samples, which demonstrated LINC00467 upregulation in 60 tumor tissue samples from patients with GC compared with that of paired para-cancerous control tissues. Functionally, LINC00467 promoted glycolysis in GC cells and enhanced their proliferative, migratory and invasive activities. From a mechanistic perspective, LINC00467 was able to bind to microRNA (miR)-141-3p in GC cells and a negative correlation between miR-141-3p and LINC00467 expression was observed in GC tissue samples. 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 and led to persistent glycolysis and GC cell invasion. The present study findings suggested that LINC00467 potentially controls GC progression via regulation of the miR-141-3p/DPYSL3 pathway.