Gut Liver.  2013 Nov;7(6):629-641.

Increasing the alpha 2, 6 Sialylation of Glycoproteins May Contribute to Metastatic Spread and Therapeutic Resistance in Colorectal Cancer

• Park JJ
• Lee M

Abstract

Abnormal glycosylation due to dysregulated glycosyltransferases and glycosidases is a key phenomenon of many malignancies, including colorectal cancer (CRC). In particular, increased ST6 Gal I (beta-galactoside alpha 2, 6 sialyltransferase) and subsequently elevated levels of cell-surface alpha 2, 6-linked sialic acids have been associated with metastasis and therapeutic failure in CRC. As many CRC patients experience metastasis to the liver or lung and fail to respond to curative therapies, intensive research efforts have sought to identify the molecular changes underlying CRC metastasis. ST6 Gal I has been shown to facilitate CRC metastasis, and we believe that additional investigations into the involvement of ST6 Gal I in CRC could facilitate the development of new diagnostic and therapeutic targets. This review summarizes how ST6 Gal I has been implicated in the altered expression of sialylated glycoproteins, which have been linked to CRC metastasis, radioresistance, and chemoresistance.

Keyword

Colorectal neoplasms; Beta-D-galactoside alpha 2-6-sialyltransferase; Neoplasm metastasis; Radioresistance; Chemoresistance

MeSH Terms

Antigens, CD/*metabolism
Colorectal Neoplasms/*metabolism/pathology/*therapy
Drug Resistance, Neoplasm
Glycoproteins/*metabolism
Humans
Liver Neoplasms/secondary
Lung Neoplasms/secondary
Radiation Tolerance
Receptor, Epidermal Growth Factor/metabolism
Sialic Acids/*metabolism
Sialyltransferases/*metabolism
Antigens, CD
Glycoproteins
Receptor, Epidermal Growth Factor
Sialic Acids
Sialyltransferases