Document Detail


Proteoglycans and their roles in brain cancer.
MedLine Citation:
PMID:  23281850     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Glioblastoma, a malignant brain cancer, is characterized by abnormal activation of receptor tyrosine kinase signalling pathways and a poor prognosis. Extracellular proteoglycans, including heparan sulfate and chondroitin sulfate, play critical roles in the regulation of cell signalling and migration via interactions with extracellular ligands, growth factor receptors and extracellular matrix components, as well as intracellular enzymes and structural proteins. In cancer, proteoglycans help drive multiple oncogenic pathways in tumour cells and promote critical tumour-microenvironment interactions. In the present review, we summarize the evidence for proteoglycan function in gliomagenesis and examine the expression of proteoglycans and their modifying enzymes in human glioblastoma using data obtained from The Cancer Genome Atlas (http://cancergenome.nih.gov/). Furthermore, we demonstrate an association between specific proteoglycan alterations and changes in receptor tyrosine kinases. Based on these data, we propose a model in which proteoglycans and their modifying enzymes promote receptor tyrosine kinase signalling and progression in glioblastoma, and we suggest that cancer-associated proteoglycans are promising biomarkers for disease and therapeutic targets.
Authors:
Anna Wade; Aaron E Robinson; Jane R Engler; Claudia Petritsch; C David James; Joanna J Phillips
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2013-02-06
Journal Detail:
Title:  The FEBS journal     Volume:  280     ISSN:  1742-4658     ISO Abbreviation:  FEBS J.     Publication Date:  2013 May 
Date Detail:
Created Date:  2013-05-10     Completed Date:  2013-07-02     Revised Date:  2014-05-07    
Medline Journal Info:
Nlm Unique ID:  101229646     Medline TA:  FEBS J     Country:  England    
Other Details:
Languages:  eng     Pagination:  2399-417     Citation Subset:  IM    
Copyright Information:
© 2013 The Authors Journal compilation © 2013 FEBS.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain Neoplasms / metabolism,  pathology*
Cell Movement
Extracellular Matrix / metabolism,  pathology
Gene Expression Regulation, Neoplastic*
Glioblastoma / metabolism,  pathology
Humans
Inflammation / metabolism,  pathology
Neovascularization, Pathologic / metabolism,  pathology
Proteoglycans / genetics,  metabolism*
Receptor, Epidermal Growth Factor / genetics,  metabolism
Receptor, Platelet-Derived Growth Factor alpha / genetics,  metabolism
Signal Transduction
Sulfotransferases / genetics,  metabolism
Tumor Microenvironment
Grant Support
ID/Acronym/Agency:
R01 CA164746/CA/NCI NIH HHS; R01 CA164746/CA/NCI NIH HHS; R01 NS080619/NS/NINDS NIH HHS; R01 NS080619/NS/NINDS NIH HHS; R01 NS081117/NS/NINDS NIH HHS; R01 NS081117/NS/NINDS NIH HHS; U01 CA168878/CA/NCI NIH HHS; U01CA168878/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Proteoglycans; EC 2.7.10.1/EGFR protein, human; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.10.1/Receptor, Platelet-Derived Growth Factor alpha; EC 2.8.2.-/SULF2 protein, human; EC 2.8.2.-/Sulfotransferases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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