ArticleFrontiers in pharmacology2026
LKB1 promotes lung adenocarcinoma cell senescence by suppressing the O-GlcNAc glycosylation-mediated activation of telomerase.
Article in Frontiers in pharmacology, 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
Background: Telomeres are crucial for maintaining genomic integrity and stability, making them promising anticancer therapy targets. O-GlcNAc glycosylation is unique and involved in most cellular functions. In most cancers, there is a positive correlation between the degree of tumor malignancy and O-GlcNAc glycosylation levels. However, the relationship between O-GlcNAc glycosylation and telomerase in lung adenocarcinoma remains unclear. We thus investigated the O-GlcNAc-mediated regulation of telomerase activity. Methods: Protein and mRNA expression levels were detected Results: Our findings revealed that LKB1 reduces the overall activity of O-GlcNAcylation and telomerase, resulting in the shortening of telomeres, increased senescence and apoptosis, and decreased tumor cell growth. Insights into the underlying mechanisms have shown that LKB1-AMPK influence the hexosamine biosynthesis pathway (HBP), potentially Discussion: O-GlcNAc glycosylation promotes telomerase activity and inhibits tumor cell senescence, thereby maintaining telomere lengths in lung adenocarcinoma tumor cells. LKB1 inhibits telomerase activity
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