LINC00852 Enhances Glycolysis and Tumor Immunity in Pancreatic Cancer via the miR‑494‑3p/GPX8 Axis.

We aimed to investigate the role and mechanism of LINC00852 in pancreatic cancer (PC), focusing on its regulation of glycolysis and tumor immunity through the miR‑494‑3p/GPX8 pathway. The expression of LINC00852, miR-494-3p, and GPX8 in PC tissues and cells was detected, and Pearson's correlation analysis was used to assess their correlations. Kaplan-Meier analysis evaluated the relationship between LINC00852 expression and patient survival. PANC-1 and AsPC-1 cells were cultured to examine proliferation, invasion, and apoptosis. Glycolysis was assessed by measuring glucose uptake and lactate production, while tumor immune function was evaluated through LDH release. A xenograft model was used to verify the in vivo oncogenic role of the LINC00852/miR-494-3p/GPX8 axis. LINC00852 and GPX8 were highly expressed in PC tissues and cells, whereas miR-494-3p showed low expression. Downregulation of LINC00852 or upregulation of miR-494-3p inhibited proliferation and invasion, promoted apoptosis, and reduced glycolysis and tumor immune capacity. Inhibition of miR-494-3p or overexpression of GPX8 partially reversed these effects. LINC00852 downregulation also suppressed tumor growth and immune evasion in mice. Mechanistically, LINC00852 bound to miR-494-3p, which directly targeted GPX8. LINC00852 facilitates glycolysis and immune evasion in PC via the miR‑494‑3p/GPX8 axis.