Affinage

GALNT6

Polypeptide N-acetylgalactosaminyltransferase 6 · UniProt Q8NCL4

Length
622 aa
Mass
71.2 kDa
Annotated
2026-06-10
29 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 4/5 claims corpus-supported (80%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GALNT6 is a Golgi-resident UDP-GalNAc:polypeptide N-acetylgalactosaminyltransferase that initiates mucin-type O-glycosylation by transferring GalNAc to serine/threonine residues of acceptor peptides, with a substrate specificity that overlaps but is functionally distinct from the closely related GALNT3 (PMID:10464263, PMID:29187600). Its glycosylation activity broadly controls the stability, localization, secretion, and signaling output of its protein substrates: it stabilizes and retains the ER chaperone GRP78/BiP (glycosylating Thr203 in the Golgi under ER stress to sustain IRE1-dependent UPR signaling) (PMID:28110670, PMID:41197411), stabilizes and confers nuclear localization on estrogen receptor alpha through site-specific glycosylation at Ser573 (PMID:30208353), and is required for the secretion and autocrine growth activity of LGALS3BP via glycosylation at Thr556/Thr571/Ser582 (PMID:31894262). Through these and related substrate modifications, GALNT6 drives oncogenic programs in multiple cancers—supporting MUC4/HER2 and MUC1/β-catenin signaling, EGFR phosphorylation, and PI3K/Akt and MEK–ERK activation—thereby promoting proliferation, invasion, epithelial-mesenchymal transition, and metastasis (PMID:28388560, PMID:27237318, PMID:30662357, PMID:32393740). In normal colon epithelium its de novo expression is sufficient to elicit dysplastic growth and disrupt differentiation and cell-cell adhesion (PMID:29187600). Beyond cancer, GALNT6 glycosylates amyloid precursor protein and reduces amyloid-β production by sterically hindering secretase cleavage (PMID:28053144).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1999 High

    Established GALNT6 as a bona fide polypeptide GalNAc-transferase, defining the enzymatic activity and showing it is not fully redundant with the highly similar GALNT3.

    Evidence In vitro enzymatic assays with defined acceptor peptides plus genomic cloning and expression analysis

    PMID:10464263

    Open questions at the time
    • Physiological substrates in vivo not identified
    • No structural basis for substrate selectivity vs GALNT3
  2. 2016 Medium

    Linked GALNT6 activity to amyloid biology by showing direct O-glycosylation of APP suppresses Aβ production, indicating glycosylation can sterically gate secretase processing.

    Evidence GALNT6 transfection in HEK293T, in vitro GalNAc-T assay on soluble APP, Aβ ELISA and secretase activity assays

    PMID:28053144

    Open questions at the time
    • Glycosylation site on APP not mapped
    • Relevance in neuronal cells/in vivo untested
  3. 2016 Medium

    Connected GALNT6 to mucin substrate stability by showing it is required for MUC4 protein/transcript levels and downstream HER2/ERK and mesenchymal phenotype.

    Evidence siRNA knockdown in pancreatic cancer cells with Western blot, RT-PCR, viability and cadherin-switching readouts

    PMID:27237318

    Open questions at the time
    • Direct glycosylation of MUC4 not biochemically demonstrated here
    • Mechanism of transcript-level change unresolved
  4. 2017 Medium

    Showed GALNT6 promotes EGFR signaling via O-glycosylation, establishing a receptor tyrosine kinase as a functional substrate-coupled output.

    Evidence VVA lectin pull-down of EGFR, siRNA knockdown, phospho-RTK array, and rescue with erlotinib in ovarian cancer cells

    PMID:28388560

    Open questions at the time
    • EGFR glycosylation sites not mapped
    • Single lab, no in vivo confirmation
  5. 2017 High

    Identified GRP78/BiP as a GALNT6 substrate and revealed a reciprocal localization loop, tying GALNT6 to ER chaperone stability and anti-apoptotic function.

    Evidence VVA lectin pull-down with mass spectrometry, co-IP, immunofluorescence localization, knockdown/overexpression apoptosis assays

    PMID:28110670

    Open questions at the time
    • Glycosylation site not defined in this study
    • Mechanism of Golgi-to-ER GALNT6 relocation unclear
  6. 2017 High

    Demonstrated causal oncogenic sufficiency: de novo GALNT6 drives dysplasia while isogenic knockout restores differentiation, and defined a GALNT6-unique substrate repertoire distinct from GALNT3.

    Evidence CRISPR knockout/rescue in isogenic colon cancer lines with quantitative O-glycoproteomics and differentiation/proliferation/adhesion assays

    PMID:29187600

    Open questions at the time
    • Which specific substrate(s) drive the dysplastic phenotype not isolated
    • In vivo tumorigenesis not addressed
  7. 2018 High

    Mapped a site-specific glycosylation event (ERα Ser573) controlling ERα stability and nuclear localization, linking GALNT6 to hormone-receptor signaling in breast cancer.

    Evidence LC-MS/MS site identification, siRNA knockdown, immunocytochemistry, co-IP, peptide competition with ERα target-gene readout

    PMID:30208353

    Open questions at the time
    • Structural mechanism by which Ser573 glycosylation governs nuclear import unknown
    • In vivo relevance to endocrine therapy untested here
  8. 2019 High

    Established that GALNT6 glycosylation at three defined sites is required for LGALS3BP secretion and autocrine growth, demonstrating mechanistic causality by mutagenesis.

    Evidence VVA pull-down, site-directed mutagenesis (T556A/T571A/S582A), secretion and proliferation assays in breast cancer cells

    PMID:31894262

    Open questions at the time
    • Receptor mediating LGALS3BP autocrine signaling not defined
    • In vivo confirmation absent
  9. 2019 Medium

    Extended GALNT6 oncogenicity to the β-catenin/MUC1-C axis through physical interaction with MUC1-N driving nuclear β-catenin and proliferative targets.

    Evidence Co-IP (GALNT6–MUC1-N; β-catenin–MUC1-C), cell fractionation, siRNA knockdown and Western blot

    PMID:30662357

    Open questions at the time
    • Direct glycosylation event not site-mapped
    • Co-IP not reciprocally validated for direct binding
  10. 2020 Medium

    Showed GALNT6 glycosylation of secreted α2M and chaperone GRP78 funnels into PI3K/Akt and MEK–ERK signaling to promote migration, invasion and EMT across cancer types.

    Evidence Glycosylomics/VVA blots, co-IP, knockdown/overexpression with PI3K/Akt and MEK/ERK Westerns and xenograft metastasis assay

    PMID:32393740 PMID:32559179

    Open questions at the time
    • Glycosylation sites on α2M and GRP78 not mapped in these studies
    • Single-lab functional readouts
  11. 2022 Medium

    Placed GALNT6 within a transcriptional circuit (RUNX3-driven) feeding MUC1 stabilization, linking upstream regulation to substrate-level output in HCC.

    Evidence Promoter binding/ChIP, RT-qPCR, knockdown and MUC1 rescue in hepatocellular carcinoma cells

    PMID:35909886

    Open questions at the time
    • MUC1 glycosylation site not defined
    • Generality of RUNX3 regulation across tissues unknown
  12. 2024 Medium

    Identified additional site-specific (PHB2 Ser161) and stabilizing substrate modifications (CCDC88C, EFEMP1) and their upstream transcriptional regulators, broadening GALNT6's substrate-stabilization paradigm.

    Evidence IP-MS, VVA lectin blots, site-directed mutagenesis (S161A), stability and metastasis assays in vitro/in vivo; LEDGF and KLF9 promoter studies

    PMID:38971758 PMID:39105355 PMID:39581475

    Open questions at the time
    • Whether stabilization is direct glycosylation-dependent for CCDC88C/EFEMP1 not site-resolved
    • Tissue specificity of upstream regulators unclear
  13. 2025 High

    Refined the GRP78 mechanism by mapping Thr203 glycosylation in the Golgi as required for GRP78–IRE1 binding and sustained UPR signaling.

    Evidence Site-directed mutagenesis (T203A), co-IP of GRP78 with IRE1, localization imaging under ER stress and proliferation assays

    PMID:41197411

    Open questions at the time
    • How Thr203 glycosylation structurally promotes IRE1 engagement unknown
    • Effect on PERK/ATF6 arms of UPR not assessed
  14. 2025 Medium

    Expanded GALNT6 function into metabolic-epigenetic reprogramming and immune evasion by stabilizing glycolytic enzymes/HIF-1α and modulating STING/PD-L1.

    Evidence Knockdown with glycolytic/metabolite/5mC measurements; STING and PD-L1 localization/degradation assays with immune co-culture

    PMID:40541816 PMID:42173327

    Open questions at the time
    • Glycosylation sites on metabolic and immune substrates not mapped
    • No in vitro reconstitution of these modifications

Open questions

Synthesis pass · forward-looking unresolved questions
  • How GALNT6 selects its broad substrate repertoire and how individual site-specific glycosylations mechanistically alter substrate folding, trafficking, and degradation remain largely unresolved.
  • No structural model of substrate recognition
  • Most reported substrates lack mapped glycosylation sites
  • In vivo physiological (non-cancer) roles minimally characterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 7 GO:0140096 catalytic activity, acting on a protein 6
Localization
GO:0005783 endoplasmic reticulum 2 GO:0005794 Golgi apparatus 2
Pathway
R-HSA-1643685 Disease 5 R-HSA-392499 Metabolism of proteins 5 R-HSA-162582 Signal Transduction 4 R-HSA-8953897 Cellular responses to stimuli 2
Partners
CCDC88CEGFRERN1ESR1HSPA5LGALS3BPMUC1PHB2

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 GALNT6 (GalNAc-T6) encodes a UDP-GalNAc:polypeptide N-acetylgalactosaminyltransferase that catalyzes O-GalNAc transfer to peptide substrates; its acceptor substrate specificities overlap with but are distinct from other GalNAc-transferases, and despite high sequence similarity to GALNT3 the two enzymes do not provide full functional redundancy. In vitro enzymatic activity assays with defined acceptor peptides; Northern analysis; immunocytology with monoclonal antibodies; genomic cloning and sequence analysis The Journal of biological chemistry High 10464263
2017 GALNT6 O-glycosylates EGFR, increasing EGFR phosphorylation and downstream signaling in ovarian cancer cells; GALNT6 knockdown reduced EGFR phosphorylation and the enhanced invasive behavior was reversed by the EGFR inhibitor erlotinib. siRNA knockdown; phospho-RTK array; Western blot; VVA lectin pull-down assay to detect O-GalNAc modification of EGFR; GALNT6 overexpression Oncotarget Medium 28388560
2016 GALNT6 directly O-glycosylates amyloid precursor protein (APP), and excess O-glycosylation of APP by GALNT6 reduces both Aβ1-40 and Aβ1-42 production without significantly altering α- or β-secretase activities, suggesting steric hindrance of secretase cleavage. Transfection of GALNT6 into HEK293T cells; in vitro GalNAc-T enzymatic activity assay on soluble APP; ELISA for Aβ; secretase activity assays Journal of biochemistry Medium 28053144
2016 GALNT6 knockdown in pancreatic cancer cells decreased MUC4 protein and transcript levels, reduced HER2 and ERK levels, suppressed viability, and caused cadherin switching from P-cadherin to E-cadherin, indicating GALNT6 O-glycosylation activity is required for MUC4 stability and maintenance of a mesenchymal phenotype. siRNA knockdown; Western blot; RT-PCR; cell viability assay; immunofluorescence for cadherin switching Neoplasia (New York, N.Y.) Medium 27237318
2017 GALNT6 O-glycosylates GRP78 (HSPA5/BiP); this O-glycosylation stabilizes GRP78 protein, retains it in the ER, and enhances its anti-apoptotic function. Conversely, overexpression of GRP78 promotes Golgi-to-ER relocation of GALNT6, indicating a reciprocal regulatory loop. VVA lectin pull-down followed by mass spectrometry to identify GRP78 as GALNT6 substrate; co-immunoprecipitation; Western blot; immunofluorescence for subcellular localization; GALNT6 knockdown/overexpression with apoptosis readout Neoplasia (New York, N.Y.) High 28110670
2017 De novo expression of GALNT6 in colon cancer cells drives a cancer-like dysplastic growth pattern; GALNT6 knockout restores more normal differentiation, reduces proliferation, and normalizes cell-cell adhesion. O-glycoproteomic analysis identified a specific set of GALNT6-unique substrates distinct from those of the closely related GALNT3. Precise gene targeting (CRISPR-based) knockout/rescue in isogenic cell lines; O-glycoproteomics; tissue culture differentiation assay; proliferation assay; cell-cell adhesion assay The Journal of biological chemistry High 29187600
2018 GALNT6 O-glycosylates estrogen receptor alpha (ERα) at Ser573 in its F domain; this modification is required for ERα protein stability and nuclear localization in breast cancer cells. GALNT6 knockdown reduces ERα protein abundance, causes loss of nuclear ERα, and downregulates ERα target genes (MYC, CCND1, CTSD). siRNA knockdown; immunocytochemistry; LC-MS/MS identification of O-glycosylation site (Ser573); co-immunoprecipitation; cell-permeable peptide competition assay Neoplasia (New York, N.Y.) High 30208353
2019 GALNT6 O-glycosylates LGALS3BP at three sites (Thr556, Thr571, Ser582); this glycosylation is required for LGALS3BP secretion and its autocrine growth-promoting activity in breast cancer. Triple alanine substitution (T556A/T571A/S582A) in LGALS3BP abolished GALNT6-dependent glycosylation, secretion, and autocrine growth. siRNA knockdown; VVA lectin pull-down; site-directed mutagenesis of glycosylation sites; secretion assay; breast cancer cell proliferation assay International journal of oncology High 31894262
2019 GALNT6 interacts with MUC1-N and promotes tumorigenicity and metastasis through the β-catenin/MUC1-C signaling pathway; GALNT6 knockdown reduces nuclear β-catenin and MUC1-C levels and decreases downstream targets PCNA, cyclin D1, and c-Myc while increasing E-cadherin. Co-immunoprecipitation (GALNT6 with MUC1-N; β-catenin with MUC1-C); cell fractionation assay; siRNA knockdown; Western blot International journal of biological sciences Medium 30662357
2020 GALNT6 O-glycosylates alpha-2-macroglobulin (α2M), and this modification activates downstream PI3K/Akt signaling to promote breast cancer cell migration and invasion. Glycosylomics analysis of supernatants from breast cancer cells; VVA lectin blot; siRNA knockdown; Western blot for PI3K/Akt; migration and invasion assays Aging Medium 32559179
2020 GALNT6 directly interacts with and O-glycosylates chaperone GRP78 in lung adenocarcinoma cells; this modification promotes epithelial-mesenchymal transition by enhancing MEK1/2–ERK1/2 signaling. Co-immunoprecipitation; VVA lectin pull-down; GALNT6 overexpression/silencing; Western blot for MEK/ERK; in vivo xenograft metastasis assay Cell death & disease Medium 32393740
2022 RUNX3 transcription factor binds the GALNT6 promoter and activates GALNT6 transcription; GALNT6-mediated O-glycosylation of MUC1 prevents its degradation and is required for HCC cell migration and invasion. Chromatin immunoprecipitation / promoter binding assay; RT-qPCR; Western blot; siRNA knockdown; MUC1 overexpression rescue experiment Disease markers Medium 35909886
2023 GALNT6 suppresses pyroptosis in pancreatic ductal adenocarcinoma by O-glycosylating NF-κB, inhibiting its nuclear translocation and thereby repressing NLRP3/GSDMD expression; additionally, GALNT6 promotes proteasomal degradation of GSDME via O-glycosylation, collectively blocking pyroptotic cell death. siRNA knockdown; Western blot; immunofluorescence for NF-κB localization; ELISA for IL-1β, IL-6, TNF-α, IL-18; scanning electron microscopy for pyroptosis morphology; qRT-PCR Frontiers in oncology Medium 36925932
2024 GALNT6 O-glycosylates prohibitin 2 (PHB2) at Ser161; this modification is required for GALNT6-induced ccRCC cell proliferation, migration, and invasion. LEDGF was identified as an upstream transcriptional inducer of GALNT6 in ccRCC. Immunoprecipitation coupled with LC-MS/MS; VVA lectin blot; site-directed mutagenesis (Ser161Ala); gain/loss-of-function experiments; in vivo xenograft; LEDGF overexpression/knockdown Cancer science High 39105355
2024 GALNT6 O-glycosylates CCDC88C, stabilizing the protein; this stabilization enables CCDC88C to drive c-JUN-mediated CEMIP transcription and promote breast cancer metastasis. Co-immunoprecipitation; VVA lectin blot; GALNT6 knockdown/overexpression; CCDC88C stability assay; in vitro and in vivo metastasis assays Cancer cell international Medium 38971758
2024 GALNT6 O-glycosylates LAPTM5, and this modification is required for LAPTM5 activity and autophagy promotion; GALNT6 also maintains the PDGFA–PDGFRB axis required for cancer-associated fibroblast activation and SPP1 secretion, contributing to lenvatinib resistance in HCC. VVA lectin assay; siRNA knockdown; Western blot; in vitro and in vivo lenvatinib sensitivity assays; TCGA-LIHC immune infiltration analysis Cellular oncology (Dordrecht, Netherlands) Medium 39718738
2024 GALNT6 O-glycosylates EFEMP1, slowing its proteasomal degradation and thereby increasing EFEMP1 protein levels; KLF9 transcription factor binds the GALNT6 promoter to suppress its transcription, placing KLF9 upstream of GALNT6 in osteosarcoma. Label-free proteomics; co-immunoprecipitation/MS; VVA lectin-based O-glycosylation assay; GALNT6 overexpression/knockdown; EFEMP1 knockdown rescue; KLF9 ChIP/promoter binding Biochimica et biophysica acta. Molecular cell research Medium 39581475
2025 GALNT6 O-glycosylates GRP78/BiP specifically at Thr203 in the Golgi apparatus (under ER stress GRP78 is transported from ER to Golgi where GALNT6 resides); substitution of Thr203 with alanine inhibits GRP78 binding to the ER stress sensor IRE1, indicating that Thr203 O-glycosylation is required for sustained UPR/IRE1 activation. Site-directed mutagenesis (Thr203Ala); co-immunoprecipitation of GRP78 with IRE1; immunofluorescence for subcellular localization under ER stress; cell proliferation assay with GALNT6 or GRP78 functional inhibition Biochemical and biophysical research communications High 41197411
2025 GALNT6 O-glycosylates and stabilizes HIF-1α, PFKM, and PKM2 (protecting them from proteasomal degradation) to promote glycolysis; simultaneously GALNT6 upregulates IDH2 and α-KGDH while suppressing GPT2, depleting α-ketoglutarate and inhibiting TET3-mediated DNA demethylation, raising 5mC levels and activating pro-tumorigenic genes such as KIF14 in TNBC. GALNT6 knockdown; glycolytic activity measurement; metabolite quantification; protein stability assays; transcriptional analysis; DNA methylation (5mC) measurement Biochimica et biophysica acta. Molecular basis of disease Medium 42173327
2025 GALNT6-mediated glycosylation blocks STING translocation and accelerates its degradation (in a cGAS-independent manner), reducing IFN-β, CCL5, and CXCL10 production; additionally, GALNT6 stabilizes PD-L1 by blocking its ubiquitin-proteasome degradation, promoting immune evasion in PDAC. siRNA knockdown; Western blot for STING, PD-L1, IFN-β; immunofluorescence for STING localization; cytokine ELISA; T cell/macrophage co-culture sensitivity assays Cellular signalling Medium 40541816

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Cloning and characterization of a close homologue of human UDP-N-acetyl-alpha-D-galactosamine:Polypeptide N-acetylgalactosaminyltransferase-T3, designated GalNAc-T6. Evidence for genetic but not functional redundancy. The Journal of biological chemistry 162 10464263
2017 De novo expression of human polypeptide N-acetylgalactosaminyltransferase 6 (GalNAc-T6) in colon adenocarcinoma inhibits the differentiation of colonic epithelium. The Journal of biological chemistry 62 29187600
2017 GALNT6 expression enhances aggressive phenotypes of ovarian cancer cells by regulating EGFR activity. Oncotarget 40 28388560
2016 Excess APP O-glycosylation by GalNAc-T6 decreases Aβ production. Journal of biochemistry 40 28053144
2016 Morphological Changes, Cadherin Switching, and Growth Suppression in Pancreatic Cancer by GALNT6 Knockdown. Neoplasia (New York, N.Y.) 39 27237318
2020 GALNT6 promotes breast cancer metastasis by increasing mucin-type O-glycosylation of α2M. Aging 38 32559179
2020 GALNT6 promotes invasion and metastasis of human lung adenocarcinoma cells through O-glycosylating chaperone protein GRP78. Cell death & disease 35 32393740
2017 GALNT6 Stabilizes GRP78 Protein by O-glycosylation and Enhances its Activity to Suppress Apoptosis Under Stress Condition. Neoplasia (New York, N.Y.) 33 28110670
2019 GALNT6 Promotes Tumorigenicity and Metastasis of Breast Cancer Cell via β-catenin/MUC1-C Signaling Pathway. International journal of biological sciences 30 30662357
2019 The GALNT6‑LGALS3BP axis promotes breast cancer cell growth. International journal of oncology 24 31894262
2019 The polypeptide GALNT6 Displays Redundant Functions upon Suppression of its Closest Homolog GALNT3 in Mediating Aberrant O-Glycosylation, Associated with Ovarian Cancer Progression. International journal of molecular sciences 20 31071912
2018 Critical Role of Estrogen Receptor Alpha O-Glycosylation by N-Acetylgalactosaminyltransferase 6 (GALNT6) in Its Nuclear Localization in Breast Cancer Cells. Neoplasia (New York, N.Y.) 19 30208353
2018 GALNT6 suppresses progression of colorectal cancer. American journal of cancer research 19 30662801
2024 GALNT6 promotes bladder cancer malignancy and immune escape by epithelial-mesenchymal transition and CD8+ T cells. Cancer cell international 15 39245709
2023 Knocking down GALNT6 promotes pyroptosis of pancreatic ductal adenocarcinoma cells through NF-κB/NLRP3/GSDMD and GSDME signaling pathway. Frontiers in oncology 14 36925932
2024 GALNT6 drives lenvatinib resistance in hepatocellular carcinoma through autophagy and cancer-associated fibroblast activation. Cellular oncology (Dordrecht, Netherlands) 10 39718738
2017 UDP-N-acetyl-D-galactosamine:polypeptide N-acetylgalactosaminyltransferase- 6 (pp-GalNAc-T6): Role in Cancer and Prospects as a Drug Target. Current cancer drug targets 10 27659430
2025 GALNT6 dual regulates innate immunity STING signaling and PD-L1 expression to promote immune evasion in pancreatic ductal adenocarcinoma. Cellular signalling 7 40541816
2024 N-acetylgalactosaminyltransferase GALNT6 is a potential therapeutic target of clear cell renal cell carcinoma progression. Cancer science 6 39105355
2024 CCDC88C, an O-GalNAc glycosylation substrate of GALNT6, drives breast cancer metastasis by promoting c-JUN-mediated CEMIP transcription. Cancer cell international 5 38971758
2022 RUNX3-Regulated GALNT6 Promotes the Migration and Invasion of Hepatocellular Carcinoma Cells by Mediating O-Glycosylation of MUC1. Disease markers 5 35909886
2021 GALNT6 Knockdown Inhibits the Proliferation and Migration of Colorectal Cancer Cells and Increases the Sensitivity of Cancer Cells to 5-FU. Journal of Cancer 3 35003361
2025 GALNT6 associated with O-GlcNAcylation contributes to the tumorigenesis of oral squamous cell carcinoma. Discover oncology 1 40659945
2025 Crucial roles of GALNT6-mediated O-glycosylation of GRP78/Bip in proliferation of breast cancer cells. Biochemical and biophysical research communications 1 41197411
2024 GALNT6, GALNT14, and Gal-3 in association with GDF-15 promotes drug resistance and stemness of breast cancer via β-catenin axis. Growth factors (Chur, Switzerland) 1 38889447
2024 GALNT6, transcriptionally inhibited by KLF9, promotes osteosarcoma progression by increasing EFEMP1 expression via O-glycosylation modification. Biochimica et biophysica acta. Molecular cell research 1 39581475
2024 Downregulation of circ_0119412 expression inhibits malignant progression of breast cancer by targeting the miR-1205/GALNT6 pathway in vivo and in vitro. Archives of medical science : AMS 1 40741237
2021 Erratum: GALNT6 Promotes Tumorigenicity and Metastasis of Breast Cancer Cell via β-catenin/MUC1-C Signaling Pathway: Erratum. International journal of biological sciences 1 34803515
2026 GALNT6 coordinates glycolysis and α-KG-dependent DNA methylation to promote TNBC progression. Biochimica et biophysica acta. Molecular basis of disease 0 42173327

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