Increasing the α 2, 6 sialylation of glycoproteins may contribute to metastatic spread and therapeutic resistance in colorectal cancer.

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 (β-galactoside α 2, 6 sialyltransferase) and subsequently elevated levels of cell-surface α 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.

• Authors: Jung-Jin Park, Minyoung Lee
• Journal: Gut and liver (Gut Liver) Vol. 7 Issue 6 Pg. 629-41 (Nov 2013) ISSN: 2005-1212 [Electronic] Korea (South)
• PMID: 24312702 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Antigens, CD
• Glycoproteins
• Sialic Acids
• Sialyltransferases
• ST6GAL1 protein, human
• ErbB Receptors

Topics

• Antigens, CD (metabolism)
• Colorectal Neoplasms (metabolism, pathology, therapy)
• Drug Resistance, Neoplasm
• ErbB Receptors (metabolism)
• Glycoproteins (metabolism)
• Humans
• Liver Neoplasms (secondary)
• Lung Neoplasms (secondary)
• Radiation Tolerance
• Sialic Acids (metabolism)
• Sialyltransferases (metabolism)