Source:http://linkedlifedata.com/resource/pubmed/id/16289236
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
19
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| pubmed:dateCreated |
2006-3-27
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| pubmed:abstractText |
Fibrinolytic factors have an important role in tumor progression through the degradation of extracellular matrix. The increased levels of urokinase-type plasminogen activator (uPA), uPA-receptor (uPAR) and type-1 PA inhibitor (PAI-1) are reported in human renal cell carcinoma (RCC). Connexin (Cx) gene, a member of gap junction, is known to act as a tumor suppressor gene. We have reported that Cx32 improves malignant phenotypes of metastatic RCC cells via the inhibition of Src-dependent signaling. In this study, we examined the effect of expression of Cx32 gene on the production of uPA, uPAR and PAI-1, and on the induction of PAI-1 stimulated by hypoxia in a human metastatic RCC cell line, Caki-1 cells. Cx32 expression decreased both mRNA level and production of PAI-1, uPA and uPAR in Caki-1 cells. Cx32 also decreased hypoxia-inducible factor (HIF)-1alpha and HIF-2alpha mRNA level. PP1, a Src inhibitor, significantly decreased PAI-1, uPA, uPAR and HIF-alpha mRNA levels in Caki-1 cells. Furthermore, Cx32 suppressed the induction of HIF-2alpha protein in Caki-1 cells under hypoxia. PAI-1 mRNA level in Cx32-transfected Caki-1 cells was lower than that of mock transfectant under hypoxic conditions. These results suggest that Cx32 might reduce PAI-1, uPA and uPAR production in metastatic RCC cells via the inhibition of Src-dependent induction of HIF-1alpha and HIF-2alpha gene expression and that Cx32 might suppress hypoxia-inducible gene expression under hypoxic conditions.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Basic Helix-Loop-Helix...,
http://linkedlifedata.com/resource/pubmed/chemical/Connexins,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoxia-Inducible Factor 1, alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/PLAUR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Plasminogen Activator Inhibitor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Urokinase Plasminogen...,
http://linkedlifedata.com/resource/pubmed/chemical/SERPINE1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Urokinase-Type Plasminogen Activator,
http://linkedlifedata.com/resource/pubmed/chemical/connexin 32,
http://linkedlifedata.com/resource/pubmed/chemical/endothelial PAS domain-containing...
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
0024-3205
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
4
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| pubmed:volume |
78
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2249-54
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16289236-Basic Helix-Loop-Helix Transcription Factors,
pubmed-meshheading:16289236-Carcinoma, Renal Cell,
pubmed-meshheading:16289236-Cell Hypoxia,
pubmed-meshheading:16289236-Cell Line, Tumor,
pubmed-meshheading:16289236-Cloning, Molecular,
pubmed-meshheading:16289236-Connexins,
pubmed-meshheading:16289236-Down-Regulation,
pubmed-meshheading:16289236-Humans,
pubmed-meshheading:16289236-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:16289236-Kidney Neoplasms,
pubmed-meshheading:16289236-Neoplasm Metastasis,
pubmed-meshheading:16289236-Plasminogen Activator Inhibitor 1,
pubmed-meshheading:16289236-Receptors, Cell Surface,
pubmed-meshheading:16289236-Receptors, Urokinase Plasminogen Activator,
pubmed-meshheading:16289236-Urokinase-Type Plasminogen Activator
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| pubmed:year |
2006
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| pubmed:articleTitle |
Connexin 32 down-regulates the fibrinolytic factors in metastatic renal cell carcinoma cells.
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| pubmed:affiliation |
Department of Food Science Research for Health, National Institute of Health and Nutrition, Toyama, Shinjuku, Tokyo, Japan. hiromi-h@nih.go.jp
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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