ArticleCellular & molecular biology letters2022
The O-glycosylating enzyme GALNT2 acts as an oncogenic driver in non-small cell lung cancer.
Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 53 citations in OpenAlex.
- Integrative bioinformatic and experimental analysis reveals prognostic and immunological roles of psychological stress-related genes in skin cutaneous melanoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- An O-glycosylation-based prognostic signature for biochemical recurrence in prostate cancer identifiesTranslational andrology and urology · 2026Article
- Integrated molecular mechanisms of salinity response in Apostichopus japonicus: focus on miRNA-driven core pathways and target gene regulation.Marine biotechnology (New York, N.Y.) · 2026Review
- GALNT7-induced O-glycosylation of NUP50 activates fatty acid β-oxidation to promote lung adenocarcinoma metastasis.The Journal of biological chemistry · 2026Article
- GALNT7 promotes the malignant progression of gastrointestinal stromal tumors by regulating KIT O-GalNAc glycosylation.Precision clinical medicine · 2026Article
- Loop of N2-polarized neutrophils and exhausted CD8 + T cells induces immunotherapy resistance in NSCLC.Molecular and cellular biochemistry · 2026Article
- The Critical Role of GALNTs-Regulated O-GalNAc Glycosylation in Cancer Malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- GalNAc-Transferases in Cancer.Biomedicines · 2025Review
- ZDHHC9 and spermine metabolism: a palmitoylation-driven pathway to prostate carcinogenesis.Journal of translational medicine · 2025Article
- Establishing and validating a new metabolic marker-driven prognosis signature for cutaneous melanoma.Scientific reports · 2025Article
- Independent validation of lung adenocarcinoma prognostic risk scores incorporating cholesterol and estrogen metabolism related transcriptional biomarkers.Scientific reports · 2025Article
- Mechanism of the GALNT family proteins in regulating tumorigenesis and development of lung cancer (Review).Molecular and clinical oncology · 2025Review
- Article
- Post-translational modifications of protein and lung cancer.Frontiers in oncology · 2025Review
- ITGA5 is associated with prognosis marker and immunosuppression in head and neck squamous cell carcinoma.Diagnostic pathology · 2024Article
- Metabolic Signaling in Cancer Metastasis.Cancer discovery · 2024Review
- GALNT2 targeted by miR-139-5p promotes proliferation of clear cell renal cell carcinoma via inhibition of LATS2 activation.Discover oncology · 2024Article
- Article
- The oncogenic role and regulatory mechanism of PGK1 in human non-small cell lung cancer.Biology direct · 2024Article
- Integrative single-cell analysis of LUAD: elucidating immune cell dynamics and prognostic modeling based on exhausted CD8+ T cells.Frontiers in immunology · 2024Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundN-Acetylgalactosaminyltransferases (GALNTs), the enzymes that initiate mucin-type O-glycosylation, are closely associated with tumor occurrence and progression. However, a comprehensive analysis of GALNTs in non-small cell lung cancer (NSCLC) is lacking.
methodsThe expression profiles and prognostic values of the GALNT family members in NSCLC were analyzed using publicly available databases. Gain- and loss-of-function experiments were applied to assess the biological function of GALNT2 in NSCLC. High-throughput sequencing and bioinformatics approaches were employed to uncover the regulatory mechanism of GALNT2.
resultsAmong the family members of GALNTs, only GALNT2 was frequently overexpressed in NSCLC tissues and was positively correlated with poor prognosis. In vitro assays showed that GALNT2 knockdown repressed NSCLC cell proliferation, migration, and invasion, but induced apoptosis and cell cycle arrest. Correspondently, GALNT2 overexpression exerted the opposite effects. In vivo experiments demonstrated that knockdown of GALNT2 restrained tumor formation in nude mice. Mechanistic investigations revealed that GALNT2 modified the O-glycosylation of ITGA5 and affected the activation of the PI3K/Akt and MAPK/ERK pathways. Further studies showed that miR-30d was a negative regulator of GALNT2.
conclusionsThese findings suggest that GALNT2 is an oncogene in NSCLC and has the potential as a target for NSCLC therapy.
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