ArticleFEBS letters2026
LncRNA YIYA drives pancreatic cancer proliferation under high-glucose conditions by reinforcing a RAS-PKM2-dependent Warburg phenotype.
Article in FEBS letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hyperglycaemia is an independent risk factor for pancreatic cancer (PC). Here, we show that both chronic and intermittent high glucose cause a robust upregulation of the novel lncRNA LINC00538 (YIYA) in pancreatic ductal adenocarcinoma (PDAC) cells. YIYA enhances PDAC cell proliferation in both 2D and 3D culture systems, and its expression shows a positive correlation with poor patient survival. Importantly, knockdown of YIYA attenuates the proliferative effect. Mechanistically, YIYA drives the Warburg phenotype in a KRAS-dependent manner. YIYA physically interacts with KRAS and the glycolytic enzyme pyruvate kinase 2 (PKM2). Notably, YIYA stabilises KRAS by preventing its autophagy-mediated degradation, thereby sustaining a proliferative state. This study identifies YIYA as a glucose-responsive lncRNA that links KRAS signalling to metabolic reprogramming in PDAC.
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