Preclinical study reveals LINC00467 knockdown suppresses glycolysis and metastasis in gastric cancer cells, highlighting a targetable miR-141-3p/DPYSL3 pathway.
Key Points
To determine the biological role, clinical expression pattern, and molecular mechanisms of the long non-coding RNA LINC00467 in gastric cancer progression.
Evaluated LINC00467 expression levels in the GEPIA database and validated them in 60 paired gastric cancer and adjacent non-cancerous control tissue samples.
Assessed gastric cancer cell proliferation, migration, invasion, and glycolytic metabolism following LINC00467 knockdown and microRNA modulation.
Investigated molecular interactions among LINC00467, miR-141-3p, the target gene DPYSL3, and AKT signaling pathway activation.
LINC00467 was significantly upregulated in gastric cancer tissues relative to paired controls, with elevated levels promoting cellular glycolysis, proliferation, migration, and invasion.
LINC00467 directly bound and sequestered miR-141-3p to increase DPYSL3 expression, and miR-141-3p inhibition reversed the antitumor effects of LINC00467 knockdown.
Glycolytic lactate accumulation triggered AKT signaling pathway activation, which enhanced LINC00467 transcription to sustain a positive feedback loop driving cancer invasion.