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Increasing the alpha 2, 6 Sialylation of Glycoproteins May Contribute to Metastatic Spread and Therapeutic Resistance in Colorectal Cancer
Gut and Liver ; : 629-641, 2013.
Article em En | WPRIM | ID: wpr-162817
Biblioteca responsável: WPRO
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.
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Texto completo: 1 Base de dados: WPRIM Assunto principal: Tolerância a Radiação / Ácidos Siálicos / Sialiltransferases / Glicoproteínas / Neoplasias Colorretais / Antígenos CD / Resistencia a Medicamentos Antineoplásicos / Receptores ErbB / Neoplasias Hepáticas / Neoplasias Pulmonares Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Revista: Gut and Liver Ano de publicação: 2013 Tipo de documento: Article
Texto completo: 1 Base de dados: WPRIM Assunto principal: Tolerância a Radiação / Ácidos Siálicos / Sialiltransferases / Glicoproteínas / Neoplasias Colorretais / Antígenos CD / Resistencia a Medicamentos Antineoplásicos / Receptores ErbB / Neoplasias Hepáticas / Neoplasias Pulmonares Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Revista: Gut and Liver Ano de publicação: 2013 Tipo de documento: Article