ArticlePrecision clinical medicine2026
GALNT7 promotes the malignant progression of gastrointestinal stromal tumors by regulating KIT O-GalNAc glycosylation.
Article in Precision clinical medicine, 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: Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract and is mainly driven by activating Methods: Bulk RNA-seq, proteomic, and single-cell RNA-seq data were integrated to identify O-glycosylation-related programs and key glycosyltransferases in GIST. Functional assays in GIST-T1 and GIST-882 cells, together with xenograft models, were performed to assess the effects of GalNAc-transferase 7 (GALNT7). GALNT7-KIT interaction, KIT O-GalNAcylation, and protein stability were examined by co-immunoprecipitation, VVA lectin blotting, confocal microscopy, and cycloheximide chase assays. Benzyl-α-GalNAc was evaluated as an O-glycosylation-targeting strategy Results: O-glycosylation signatures were enriched in high-risk GIST and correlated with pathological risk. High O-glycosylation scores co-segregated with elevated copy-number variation in a fibroblast-like malignant cell population. Conclusions: GALNT7-mediated O-GalNAc glycosylation stabilizes KIT and drives GIST progression. GALNT7 may serve as a prognostic biomarker and therapeutic target in GIST.
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