β1, 4-N-acetylgalactosaminyltransferase III modulates cancer stemness through EGFR signaling pathway in colon cancer cells.

Cancer stem cells are cancer cells characterized with tumor initiating capacity. β1,4-N-acetylgalactosaminyltransferase III (B4GALNT3) synthesizes GalNAcβ1-4GlcNAc (LacdiNAc) which contributes to self-renewal of mouse embryonic stem cells. We previously showed that B4GALNT3 overexpression enhances colon cancer cell malignant phenotypes in vitro and in vivo.

B3GNT3 expression suppresses cell migration and invasion and predicts favorable outcomes in neuroblastoma.

Aberrant expression of the simple mucin-type carbohydrate antigens such as T, Tn, sialyl-T and sialyl-Tn is associated with poor prognosis in several cancers. β1,3-N-acetylglucosaminyltransferase-3 (B3GNT3), a member of the β3GlcNAcT family, is responsible for forming extended core 1 (T antigen) oligosaccharides. The role of B3GNT3, which is expressed in various tissues including human fetal brain, in regulating neuroblastoma (NB) formation and cell behaviors remains unclear.

β-1,4-Galactosyltransferase III enhances invasive phenotypes via β1-integrin and predicts poor prognosis in neuroblastoma.

Purpose: Neuroblastoma (NB) is a neural crest-derived tumor that commonly occurs in childhood. β-1,4-Galactosyltransferase III (B4GALT3) is highly expressed in human fetal brain and is responsible for the generation of poly-N-acetyllactosamine, which plays a critical role in tumor progression. We therefore investigated the expression and role of B4GALT3 in NB.

The molecular chaperone Cosmc enhances malignant behaviors of colon cancer cells via activation of Akt and ERK.

Expression of T antigen (Galbeta1, 3GalNAc) is associated with enhanced metastatic potential and poor prognosis in colorectal cancer. Cosmc is a molecular chaperone required for the formation of an active T-synthase, which catalyzes the synthesis of T antigen. However, the expression and role of Cosmc in colorectal cancer are still unclear.

B4GALNT3 expression predicts a favorable prognosis and suppresses cell migration and invasion via β₁ integrin signaling in neuroblastoma.

β1,4-N-acetylgalactosaminyltransferase III (B4GALNT3) promotes the formation of GalNAcβ1,4GlcNAc (LacdiNAc or LDN). Drosophila β1,4-N-acetylgalactosaminyltransferase A (B4GALNTA) contributes to the synthesis of LDN, which helps regulate neuronal development. In this study, we investigated the expression and role of B4GALNT3 in human neuroblastoma (NB).

Overexpression of MUC15 activates extracellular signal-regulated kinase 1/2 and promotes the oncogenic potential of human colon cancer cells.

Mucins play a key role in tumorigenesis. MUC15 is a membrane-bound mucin and the MUC15 messenger RNA (mRNA) has been detected in various organs. However, its role in tumor malignancy is still unclear.

Beta1,4-N-acetylgalactosaminyltransferase III enhances malignant phenotypes of colon cancer cells.

The enzyme beta1,4-N-acetylgalactosaminyltransferase III (beta4GalNAc-T3) exhibits in vitro activity of synthesizing N,N'-diacetyllactosediamine, GalNAcbeta1,4GlcNAc. Here, we investigate the expression of beta4GalNAc-T3 in primary colon tumors and the effects of its overexpression on HCT116 colon cancer cells. Real-time reverse transcription-PCR showed that the expression of beta4GalNAc-T3 was up-regulated in 72.