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• W2024610129 abstract "Angiogenesis, which is the process of sprouting of new blood vessels from pre-existing vessels, is vital for tumor progression. Proteolytic remodeling of extracellular matrix is a key event in vessel sprouting during angiogenesis. Urokinase type plasminogen activator receptor (uPAR) and cathepsin B are both known to be overexpressed and implicated in tumor angiogenesis. In the present study, we observed that knockdown of uPAR and cathepsin B using puPAR (pU), pCathepsin B (pC), and a bicistronic construct of uPAR and cathepsin B (pCU) caused significant inhibition of angiogenesis by disrupting the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway-dependent expression of vascular endothelial growth factor (VEGF). Further, transcriptional suppression of uPAR and cathepsin B inhibited tumor-induced migration, proliferation of endothelial cells and decreased tumor-promoted expression of VEGF receptor-2, Rac1, gp91phox, cyclin D1, cyclin dependent kinase 4 and p-Rb in human dermal microvascular endothelial cell. Furthermore, U251 and SNB19 xenograft tissue sections from nude mice treated with pCU showed reduced expression of VEGF and CD31, which is a blood vessel visualization marker. Overall, results revealed that knockdown of uPAR and cathepsin B inhibited tumor-induced angiogenesis by disrupting the JAK/STAT pathway-dependent expression of VEGF. These data provide new insight in characterizing the pathways involved in the angiogenic cascade and for the identification of novel target proteins for use in therapeutic intervention for gliomas." @default.
• W2024610129 created "2016-06-24" @default.
• W2024610129 creator A5006284247 @default.
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• W2024610129 date "2011-03-11" @default.
• W2024610129 modified "2023-10-12" @default.
• W2024610129 title "Cathepsin B and uPAR knockdown inhibits tumor-induced angiogenesis by modulating VEGF expression in glioma" @default.
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• W2024610129 cites W1576290062 @default.
• W2024610129 cites W157839118 @default.
• W2024610129 cites W1607080847 @default.
• W2024610129 cites W1679229092 @default.
• W2024610129 cites W1805256772 @default.
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• W2024610129 cites W1978041336 @default.
• W2024610129 cites W1980013575 @default.
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• W2024610129 doi "https://doi.org/10.1038/cgt.2011.9" @default.
• W2024610129 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3096680" @default.
• W2024610129 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21394106" @default.
• W2024610129 hasPublicationYear "2011" @default.
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