ArticleActa biochimica et biophysica Sinica2025
GALNT7 promotes hepatocellular carcinoma progression by activating the PI3K/AKT signaling pathway via O-glycosylation of MUC13.
Article in Acta biochimica et biophysica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Cancer-associated alterations in O-GalNAc glycosylation.Glycobiology · 2026Review
- ACSL1 orchestrates ferroptosis and degranulation in low-density neutrophils: a novel pathogenic mechanism and therapeutic target in systemic lupus erythematosus.Molecular and cellular biochemistry · 2026Article
- GALNT7-induced O-glycosylation of NUP50 activates fatty acid β-oxidation to promote lung adenocarcinoma metastasis.The Journal of biological chemistry · 2026Article
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13 authors.
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Abstract
Hepatocellular carcinoma (HCC) represents a significant global health challenge due to its aggressive malignancy. Abnormal glycosylation is a frequent phenomenon in tumor cells and manifests as alterations in key cancer biomarkers. This phenomenon is driven primarily by changes in the expressions of glycosyltransferases. Our study focuses on GALNT7, a member of the GALNT glycosyltransferase family, which catalyzes the initiation of O-linked glycan synthesis by transferring N-acetylgalactosamine (GalNAc) to serine or threonine residues on target proteins. We observe that GALNT7 expression is notably increased in HCC tissues and is correlated with increased tumor cell invasion, migration, and proliferation, alongside with reduced apoptosis, both
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