Skip Navigation


Glycobiology Advance Access originally published online on September 26, 2003
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
14/1/39    most recent
cwh002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (9)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Dall'Olio, F.
Right arrow Articles by Grigioni, W. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dall'Olio, F.
Right arrow Articles by Grigioni, W. F.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Glycobiology vol 14 no 1 pp. 39-49, 2004
© Oxford University Press 2004; all rights reserved.

Expression of ß-galactoside {alpha}2,6 sialyltransferase and of {alpha}2,6-sialylated glycoconjugates in normal human liver, hepatocarcinoma, and cirrhosis

Fabio Dall'Olio1,2, Mariella Chiricolo2, Antonia D'Errico3, Elisa Gruppioni3, Annalisa Altimari3, Michelangelo Fiorentino3 and Walter F. Grigioni3

2 Department of Experimental Pathology, F. Addarii Institute of Oncology, University of Bologna, Via S. Giacomo 14, 40126 Bologna, Italy; and 3 Pathology Unit, F. Addarii Institute of Oncology, University of Bologna, Bologna, Italy

Received on July 22, 2003; revised on September 2, 2003; accepted on September 2, 2003

ß-Galactoside {alpha}2,6-sialyltransferase (ST6Gal.I) mediates the addition of {alpha}2,6-linked sialic acid to glycoproteins. ST6Gal.I is strongly expressed by the liver and is up-regulated in several cancers, but little is known of its regulation in human liver diseases. We have investigated the expression of ST6Gal.I and its product, the {alpha}2,6-sialylated lactosamine, in normal human liver, hepatocarcinoma (HCC), and cirrhosis. We found that both ST6Gal.I activity and mRNA can undergo up- or down-regulation in different HCC patients. At the mRNA level, the groups of specimens showing the highest expression were HCC of grade 2, HCC developed without preexisting cirrhosis, and HCC of male patients. The lectin from Sambucus nigra (SNA) reveals a significative overexpression of {alpha}2,6-sialylated glycoconjugates in HCC tissue homogenates and their intracellular accumulation in HCC histological sections, even though in a few cases the extent of {alpha}2,6-sialylation dramatically decreases. Transcription of the gene occurs through at least two different promoters, resulting in two differentially expressed mRNA species. RNA in situ hybridization reveals that the ST6Gal.I mRNA can be expressed at a quantitatively heterogeneous level among the neoplastic cells. Neither ST6Gal.I expression nor {alpha}2,6-sialylation are altered in cirrhosis. These data indicate that neoplastic transformation but not cirrhosis can alter the process of {alpha}2,6-sialylation of liver glycoproteins.

1 To whom correspondence should be addressed; e-mail: dallolio{at}alma.unibo.it


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
BloodHome page
M. Nasirikenari, B. H. Segal, J. R. Ostberg, A. Urbasic, and J. T. Lau
Altered granulopoietic profile and exaggerated acute neutrophilic inflammation in mice with targeted deficiency in the sialyltransferase ST6Gal I
Blood, November 15, 2006; 108(10): 3397 - 3405.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.