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Literature summary for 2.4.1.150 extracted from

  • Zhang, H.; Meng, F.; Wu, S.; Kreike, B.; Sethi, S.; Chen, W.; Miller, F.R.; Wu, G.
    Engagement of I-branching beta-1,6-N-acetylglucosaminyltransferase 2 in breast cancer metastasis and TGF-beta signaling (2011), Cancer Res., 71, 4846-4856 .
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Application

Application Comment Organism
medicine GCNT2 is overexpressed in highly metastatic breast cancer and its expression correlates with adverse pathologic phenotypes. Blocking TGF-beta/GCNT2 signaling is a promising approach for targeting metastatic breast cancer Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens Q8N0V5
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Source Tissue

Source Tissue Comment Organism Textmining
breast cancer cell GCNT2 is overexpressed in highly metastatic breast cancer cell lines. GCNT2 expression is also significantly correlated to the metastatic phenotype in breast tumor samples Homo sapiens
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BT-20 cell
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 Homo sapiens
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MCF-7 cell
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 Homo sapiens
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MDA-MB-231 cell
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 Homo sapiens
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MDA-MB-361 cell
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 Homo sapiens
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MDA-MB-435 cell
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 Homo sapiens
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Synonyms

Synonyms Comment Organism
GCNT2
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 Homo sapiens
glucosaminyl (N-acetyl) transferase 2
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 Homo sapiens
I-branching beta-1,6-N-acetylglucosaminyl transferase 2
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 Homo sapiens
I-branching enzyme
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 Homo sapiens

General Information

General Information Comment Organism
malfunction ectopic overexpression of GCNT2 enhances cell detachment, adhesion to endothelial cells, cell migration and invasion in vitro, and lung metastasis of breast cancer cells in vivo. Knockdown of GCNT2 expression decreases cell migration and invasion in vitro and lung metastasis in vivo. Diminution of the glycosyltransferase activity of I-branching beta-1,6-N-acetylglucosaminyl transferase 2 (GCNT2) abrogates its cell migration and invasion-promoting function and synergistic effect with TGF-beta to induce EMT, effect of GCNT2 expression knockdown on oncogenic properties, overview Homo sapiens
metabolism GCNT2 is a direct target of the TGF-beta-smad pathway and that change in GCNT2 expression modulates EMT induced by TGF-beta1 treatment. Involvement of GCNT2 in EMT and TGF-beta signaling, and further glycosylation modification of E-cadherin by GCNT2, are the underlying integrative mechanisms for breast cancer metastasis. GCNT2 contributes to distal metastasis in vivo Homo sapiens
physiological function GCNT2 is a gene contributing to breast cancer metastasis with preferential expression in basal-like breast cancer. GCNT2 induces epithelial-mesenchymal transition and promotes migration and invasion in esophageal squamous cell carcinoma cells. Involvement of GCNT2 in the epithelial-to-mesenchymal transition (EMT). Specifically, the expression of E-cadherin is significantly changed upon GCNT2 expression at the protein level but not at the RNA level Homo sapiens