Document Detail

Reduced syndecan-1 expression stimulates heparin-binding growth factor-mediated invasion in ovarian cancer cells in a urokinase-independent mechanism.
MedLine Citation:
PMID:  16012729     Owner:  NLM     Status:  MEDLINE    
The expression of syndecan-1 generally appears down-regulated in human cancers and experimental models, whereas transfectional expression of syndecan-1 in cancer cells has been shown to inhibit aspects of their malignant behavior. To clarify how reduced levels of syndecan-1 may confer enhanced invasiveness, we transfected human ovarian cancer cell line HRA with antisense (AS) syndecan-1 oligodeoxynucleotide (ODN) and compared the properties of transfected cells to those of parental cells or sense (S) syndecan-1 cells. Here, we show: 1) there was lower proliferation in the AS syndecan-1 cells compared to controls (parental HRA cells and S syndecan-1 cells) when cells were incubated with HB-GFs (HB-EGF, HGF, or FGF2); 2) transfection of HRA cells with a syndecan-1 AS ODN enhanced the increase in HB-GF-dependent invasiveness; 3) in contrast, IGF-I stimulated cell proliferation and invasion, irrespective of whether cells were transfected with the AS syndecan-1 gene; 4) IGF-I stimulated ERK1/2 activation and uPA expression in both the control and AS cells, whereas the net effect of the reduction of syndecan-1 is to shift the HB-GF dose-response curve to the right; 5) the AS cells reduced activation and up-regulation of ERK1/2 phosphorylation and uPA expression, respectively, in response to HB-GFs; and 6) in comparison with early stage ovarian cancer tissues, there was a 3-fold decrease in syndecan-1 mRNA levels in advanced stage tissues. Taken together, these data suggest that decreased syndecan-1 expression may be associated with enhanced cell invasion possibly through the uPA-independent mechanism.
Hidenori Matsuzaki; Hiroshi Kobayashi; Tatsuo Yagyu; Kiyoshi Wakahara; Toshiharu Kondo; Noriyuki Kurita; Hideo Sekino; Kiyokazu Inagaki; Mika Suzuki; Naohiro Kanayama; Toshihiko Terao
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncology reports     Volume:  14     ISSN:  1021-335X     ISO Abbreviation:  Oncol. Rep.     Publication Date:  2005 Aug 
Date Detail:
Created Date:  2005-07-13     Completed Date:  2005-09-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9422756     Medline TA:  Oncol Rep     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  449-57     Citation Subset:  IM    
NetForce Co. Ltd., Taiko 3-1-18, Nakamura, Nagoya, Aichi 453-0801, Japan.
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MeSH Terms
Blotting, Northern
Blotting, Western
Cell Line, Tumor
Cell Movement / drug effects
Cell Proliferation / drug effects
Dose-Response Relationship, Drug
Down-Regulation / drug effects,  genetics
Fibroblast Growth Factor 1 / pharmacology
Fibroblast Growth Factor 2 / pharmacology
Fibroblast Growth Factors / pharmacology*
Gene Expression Regulation, Enzymologic / drug effects
Gene Expression Regulation, Neoplastic / drug effects
Insulin-Like Growth Factor I / pharmacology
Membrane Glycoproteins / genetics*
Middle Aged
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Neoplasm Invasiveness
Neoplasm Staging
Oligonucleotides, Antisense / genetics
Ovarian Neoplasms / genetics,  metabolism,  pathology*
Phosphorylation / drug effects
Proteoglycans / genetics*
RNA, Messenger / genetics,  metabolism
Urokinase-Type Plasminogen Activator / genetics*
Reg. No./Substance:
0/Membrane Glycoproteins; 0/Oligonucleotides, Antisense; 0/Proteoglycans; 0/RNA, Messenger; 0/SDC1 protein, human; 0/Syndecan-1; 0/Syndecans; 103107-01-3/Fibroblast Growth Factor 2; 104781-85-3/Fibroblast Growth Factor 1; 62031-54-3/Fibroblast Growth Factors; 67763-96-6/Insulin-Like Growth Factor I; EC Protein Kinase 1; EC Protein Kinase 3; EC Plasminogen Activator

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