GALNT6

Last update 08 May 2025

Basic Info

Synonyms

GalNAc-T6, GALNT6, Polypeptide GalNAc transferase 6

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Introduction

Catalyzes the initial reaction in O-linked oligosaccharide biosynthesis, the transfer of an N-acetyl-D-galactosamine residue to a serine or threonine residue on the protein receptor (PubMed:10464263, PubMed:31932717). May participate in synthesis of oncofetal fibronectin (PubMed:10464263). Has activity toward MUC1A, MUC2, EA2 and fibronectin peptides (PubMed:10464263). Glycosylates FGF23 (PubMed:31932717).

100 Clinical Results associated with GALNT6

100 Translational Medicine associated with GALNT6

0 Patents (Medical) associated with GALNT6

Literatures (Medical) associated with GALNT6

01 Feb 2025·Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

GALNT6, transcriptionally inhibited by KLF9, promotes osteosarcoma progression by increasing EFEMP1 expression via O-glycosylation modification

Article

Author: Shen, Yuan ; Yuan, Quan ; Yu, Honghao ; Tong, Ziyuan

Osteosarcoma (OS) is one of the deadliest malignancies in adolescents and its treatment status and prognosis remain unsatisfactory. N-acetylgalactosamine transferase 6 (GALNT6), one of the key enzymes regulating O-glycosylation, functions vary in different types of cancer. Currently, the function of GALNT6 in OS is unclear. Our results showed that GALNT6 was highly expressed in OS tissues, and the patients with higher GALNT6 expression exhibited a lower overall survival rate than patients with lower GALNT6 expression. We constructed the GALNT6-knockdown and GALNT6-overexpression vectors based on Tet-on system and packaged lentiviral particles to modulate GALNT6 expression. GALNT6 silencing impaired OC cell growth and metastasis both in vivo and vitro. Kruppel-like factor 9 (KLF9), a transcription factor known to suppress OS progression, was found to block GALNT6 transcription by binding to its promoter. Meanwhile, GALNT6 overexpression restored the effects caused by KLF9 upregulation. GALNT6 was known to affect protein stability by O-glycosylation regulation, thus the label-free proteomics combined with co-immunoprecipitation/mass-spectrum (MS) analysis were conducted to identify the potential mechanism of GALNT6 in promoting OS progression. EGF-containing fibulin extracellular matrix protein 1 (EFEMP1), contained several O-glycosylation sites and was upregulated in GALNT6 overexpressing cells (Log₂FC = 1.3195, p = 0.0160), attracted our attention. We demonstrated that GALNT6 interacted with EFEMP1 at protein level. The O-glycosylation of EFEMP1 was increased by GALNT6 overexpression, which slowed the degradation rate of EFEMP1. EFEMP1 knockdown reversed the effects of GALNT6 overexpression. Collectively, our observations demonstrate that KLF9/GALNT6/EFEMP1 may be a promising direction for OS treatment.

01 Feb 2025·Arteriosclerosis, Thrombosis, and Vascular Biology

Single-Cell Transcriptomics Identifies Selective Lineage-Specific Regulation of Genes in Aortic Smooth Muscle Cells in Mice

Article

Author: Liu, Li ; Lee, Chloe Y. ; Jana, Sayantan ; Dichek, David A. ; Quertermous, Thomas ; Shukla, Shalabh ; Cheng, Paul ; Sanford, Nicole

BACKGROUND:Smooth muscle cells (SMCs) of the proximal thoracic aorta are derived from second heart field (SHF) and cardiac neural crest (CNC) lineages. Recent studies, both in vitro and in vivo, have implied relevance of lineage-specific SMC functions in the pathophysiology of thoracic aortic diseases; however, whether 2 lineage-derived SMCs have any predisposed transcriptional differences in the control aorta remains unexplored.METHODS: Single-cell RNA sequencing and single-nucleus assay for transposase-accessible chromatin sequencing were performed on isolated cells from the aortic root and ascending aortas of 14-week-old SHF-traced ( Mef2c-Cre+/0-Yfp+/0 ) and CNC-traced ( Wnt1-Cre+/0-Yfp+/0 ) male mice. RNA in situ hybridization was performed for spatial expression of selected differentially expressed genes (DEGs) of both lineages. RESULTS: Lineage stratification of SMCs in the proximal thoracic aorta was identified using antibody-based immunofluorescence staining. Single-cell RNA sequencing recognized 12 consistently upregulated DEGs ( Des , Tnnt2 , Hand2os1 , Psd , Gpc3 , Meis2 , Dcn , Gm34030 , Palld , Nrtn , Lum , and Cfh ) in SHF-derived SMCs and 9 consistently upregulated DEGs ( Ccn5 , Ccdc42 , Tes , Eln , Aebp1 , Galnt6 , Ccn2 , Aopep , and Wtip ) in CNC-derived SMCs. RNA in situ hybridization validated upregulated expressions of selective SHF-specific DEGs at the aortic root. We found SHF-derived SMCs contain a distinct, large subpopulation of SMCs that is enriched with Des and Tnnt2 expressions. Single-nucleus assay for transposase-accessible chromatin analysis further confirmed higher chromosomal accessibility for upregulated DEGs of SHF-derived SMCs. CONCLUSIONS:The present study recognizes the presence of limited but distinct transcriptomic differences between CNC-derived and SHF-derived SMCs in the control proximal thoracic aorta.

01 Dec 2024·Cellular Oncology

GALNT6 drives lenvatinib resistance in hepatocellular carcinoma through autophagy and cancer-associated fibroblast activation

Article

Author: Yang, Yi ; Wan, Jinglei ; Wang, Biao ; Quan, Bing ; Zhou, Zhengjun ; Song, Lina ; Cai, Jialiang ; Li, Tao ; Chen, Shiping ; Zhu, Guiqi ; Zhang, Peiling ; Dai, Zhi

BACKGROUNDHepatocellular carcinoma (HCC) remains a significant global health challenge with limited treatment options. Lenvatinib, a tyrosine kinase inhibitor, has shown promise but is often undermined by the development of drug resistance.METHODSUtilizing high-throughput sequencing, we investigated the molecular mechanisms underlying lenvatinib resistance in HCC cells, with a focus on metabolic pathways. Key genes, including GALNT6, were validated through quantitative real-time PCR. The effects of GALNT6 knockdown on lenvatinib sensitivity were examined in vitro and in vivo. O-GalNAc glycosylation was assessed using Vicia Villosa Lectin. Immune cell infiltration and interactions were analyzed in the TCGA-LIHC cohort, with further validation by Western blotting and immunohistochemistry.RESULTSOur findings indicate that lenvatinib resistance in HCC is driven by the mucin-type O-glycosylation pathway, with GALNT6 playing a critical role. Knockdown of GALNT6 led to reduced O-GalNAc glycosylation, including the modification of LAPTM5, resulting in decreased LAPTM5 activity and autophagy inhibition. Additionally, GALNT6 silencing disrupted the PDGFA-PDGFRB axis, impairing the activation of cancer-associated fibroblasts (CAFs) and reducing their secretion of SPP1, which collectively diminished lenvatinib resistance.CONCLUSIONSGALNT6 is integral to the resistance mechanisms against lenvatinib in HCC by modulating autophagy and CAF activation. Targeting GALNT6 offers a promising strategy to enhance lenvatinib efficacy and improve therapeutic outcomes in HCC.

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GALNT6

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