Table 1 Key enzymes involved in the cancer-associated N- and O-glycosylation pathway

Β-galactoside α2,6-sialyltransferase I (ST6Gal-I)

A dds sialic acid to the terminal galactose of N-glycosylated proteins. Mediates synthesis of α2,6-sialylated lactosamine (Sia6LacNAc)

Altered expression in various malignancies including colon and ovarian cancer

[42]

Fucosyltransferase VIII (Fuc-TVIII)

Catalyzes the addition of fucose in alpha 1–6 linkage to the innermost GlcNAc residue of an N-linked glycoproteins and mediates core fucosylation

Overexpression of this enzyme is associated with tumor development and progression in lung cancer and breast cancer

[43,44,45]

Fucosyltransferase VII (Fuc-TVII)

Mediates terminal fucosylation (addition of Fuc in α1,3 linkage to an α2,3-sialylated type 2 chain and giving rise to specific Lewis antigens, such as SLe^x)

Enhanced expression of SLe^x in adult T cell leukemia cells has been shown to be dependent on Fuc-TVII activity

[46]

Fucosyltransferase VI (Fuc-TVI)

Mediates terminal fucosylation (addition of Fuc in α1,3 linkage to an α2,3-sialylated type 2 chain)

Altered expression in breast cancer

[47]

N-acetylglucosamine transferases (β1,3GlcNAc transferase)

I nitiates production of the Lacto series that can carry multiple glycan epitopes such as blood group antigens

Altered expression in colon cancer

[48]

N-acetylglucosaminyltransferase V (GnT-V)

Responsible for branching GlcNAc N-glycans

GnT-V-mediated glycosylation regulates the colon cancer stem cell compartment and tumor progression

[49]

N-acetylglucosaminyltransferase III (GnT-III)

Catalyzes the addition of bisecting GlcNAc N-glycans in a β1,4-linkage, suppressing additional elongation of N-glycans such as the β1,6-branching structures

Involved in the suppression of lung cancer metastasis

[50]