Increasing the alpha 2, 6 Sialylation of Glycoproteins May Contribute to Metastatic Spread and Therapeutic Resistance in Colorectal Cancer.
- Author:
Jung Jin PARK
1
;
Minyoung LEE
Author Information
1. Division of Life Science, Korea University College of Life Sciences and Biotechnology, Seoul, Korea.
- Publication Type:Review ; Research Support, Non-U.S. Gov't
- Keywords:
Colorectal neoplasms;
Beta-D-galactoside alpha 2-6-sialyltransferase;
Neoplasm metastasis;
Radioresistance;
Chemoresistance
- MeSH:
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
- From:Gut and Liver
2013;7(6):629-641
- CountryRepublic of Korea
- Language:English
-
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.
