FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2012532921> ?p ?o ?g. }

• W2012532921 endingPage "47" @default.
• W2012532921 startingPage "33" @default.
• W2012532921 abstract "The uPA/uPAR system is known to play a critical role in angiogenesis of glioblastoma. Previously, we have shown that shRNA against uPA and uPAR attenuates angiogenesis by blocking nuclear translocation of angiogenin, inhibition of angiopoietin/Tie2 signaling, and regulating several other pro‐angiogenic, angiostatic and anti‐angiogenic molecules. Further analysis revealed that GM‐CSF, a pleiotropic cytokine, was significantly inhibited in U87MG and 4910 co‐cultures with endothelial cells transfected with shRNA against uPA and uPAR. The role of the uPA/uPAR system in this process is not completely understood. Analysis of tumor conditioned medium of U87MG, 4910 and HMECs transfected with shRNA against uPA or uPAR alone or in combination (pU2) revealed inhibition of GM‐CSF‐enhanced secretion of SVEGFR1 as shown by Western blotting and ELISA. Moreover, phosphorylation of JAK2 and STAT5, the downstream effectors of GM‐CSF signaling, was also inhibited in all three cell lines. Phosphorylation at Tyr 166 position of the GM‐CSFRβ subunit, the signal activating subunit of the GM‐CSF receptor, was inhibited in HMEC, U87MG and 4910 cells. Further analysis revealed that shRNA against uPA and/or uPAR increased secretion of TIMP‐1, which is known to enhance SVEGFR1 secretion in endothelial cells. Moreover, addition of purified uPA (with and without GM‐CSF) activated JAK2/STAT5 signaling in HMEC. Exogenous addition of SVEGFR1 to pU2 tumor conditioned medium enhanced inhibition of VEGF‐induced endothelial capillary tube formation as assessed by an in vitro angiogenesis assay. To determine the significance of these events in vivo, nude mice with pre‐established tumors treated with shRNA against uPA and/or uPAR showed decreased levels of GM‐CSF and increased levels of SVEGFR1 and TIMP‐1 when compared with controls. Enhanced secretion of SVEGFR1 by puPA, puPAR and pU2 in endothelial and GBM cells was mediated indirectly by MMP‐7 and augmented by ectodomain shedding of VEGFr1 by tyrosine phosphorylation at the 1213 position. Taken together, these results suggest that the uPA/uPAR system could prove beneficial as an indirect target for inhibition of angiogenesis in glioblastoma." @default.
• W2012532921 created "2016-06-24" @default.
• W2012532921 creator A5002976501 @default.
• W2012532921 creator A5010004856 @default.
• W2012532921 creator A5024252918 @default.
• W2012532921 creator A5059893021 @default.
• W2012532921 creator A5063197597 @default.
• W2012532921 creator A5071514249 @default.
• W2012532921 date "2011-11-30" @default.
• W2012532921 modified "2023-09-27" @default.
• W2012532921 title "uPA and uPAR shRNA inhibit angiogenesis via enhanced secretion of SVEGFR1 independent of GM-CSF but dependent on TIMP-1 in endothelial and glioblastoma cells" @default.
• W2012532921 cites W18563431 @default.
• W2012532921 cites W1905974666 @default.
• W2012532921 cites W1963681491 @default.
• W2012532921 cites W1964361275 @default.
• W2012532921 cites W1967638202 @default.
• W2012532921 cites W1970058214 @default.
• W2012532921 cites W1973343326 @default.
• W2012532921 cites W1981520514 @default.
• W2012532921 cites W1990646545 @default.
• W2012532921 cites W1995570995 @default.
• W2012532921 cites W1999669021 @default.
• W2012532921 cites W2010576677 @default.
• W2012532921 cites W2021064931 @default.
• W2012532921 cites W2028085190 @default.
• W2012532921 cites W2031707630 @default.
• W2012532921 cites W2041829432 @default.
• W2012532921 cites W2048777223 @default.
• W2012532921 cites W2056146626 @default.
• W2012532921 cites W2058902820 @default.
• W2012532921 cites W2063726066 @default.
• W2012532921 cites W2064783491 @default.
• W2012532921 cites W2075172358 @default.
• W2012532921 cites W2077123765 @default.
• W2012532921 cites W2078474641 @default.
• W2012532921 cites W2080906856 @default.
• W2012532921 cites W2086026895 @default.
• W2012532921 cites W2089231072 @default.
• W2012532921 cites W2092565468 @default.
• W2012532921 cites W2096009880 @default.
• W2012532921 cites W2103248971 @default.
• W2012532921 cites W2103553030 @default.
• W2012532921 cites W2111172085 @default.
• W2012532921 cites W2119499788 @default.
• W2012532921 cites W2124235176 @default.
• W2012532921 cites W2125014313 @default.
• W2012532921 cites W2131515450 @default.
• W2012532921 cites W2135351121 @default.
• W2012532921 cites W2141222526 @default.
• W2012532921 cites W2141494367 @default.
• W2012532921 cites W2141919376 @default.
• W2012532921 cites W2146519773 @default.
• W2012532921 cites W2148803067 @default.
• W2012532921 cites W2155372340 @default.
• W2012532921 cites W2165674359 @default.
• W2012532921 cites W2168231999 @default.
• W2012532921 cites W2168439008 @default.
• W2012532921 cites W2169424184 @default.
• W2012532921 cites W2288126169 @default.
• W2012532921 cites W2299336915 @default.
• W2012532921 cites W4231451806 @default.
• W2012532921 doi "https://doi.org/10.1016/j.molonc.2011.11.008" @default.
• W2012532921 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3268919" @default.
• W2012532921 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22177802" @default.
• W2012532921 hasPublicationYear "2011" @default.
• W2012532921 type Work @default.
• W2012532921 sameAs 2012532921 @default.
• W2012532921 citedByCount "25" @default.
• W2012532921 countsByYear W20125329212012 @default.
• W2012532921 countsByYear W20125329212013 @default.
• W2012532921 countsByYear W20125329212014 @default.
• W2012532921 countsByYear W20125329212015 @default.
• W2012532921 countsByYear W20125329212017 @default.
• W2012532921 countsByYear W20125329212018 @default.
• W2012532921 countsByYear W20125329212019 @default.
• W2012532921 countsByYear W20125329212020 @default.
• W2012532921 countsByYear W20125329212021 @default.
• W2012532921 countsByYear W20125329212022 @default.
• W2012532921 countsByYear W20125329212023 @default.
• W2012532921 crossrefType "journal-article" @default.
• W2012532921 hasAuthorship W2012532921A5002976501 @default.
• W2012532921 hasAuthorship W2012532921A5010004856 @default.
• W2012532921 hasAuthorship W2012532921A5024252918 @default.
• W2012532921 hasAuthorship W2012532921A5059893021 @default.
• W2012532921 hasAuthorship W2012532921A5063197597 @default.
• W2012532921 hasAuthorship W2012532921A5071514249 @default.
• W2012532921 hasBestOaLocation W20125329211 @default.
• W2012532921 hasConcept C11960822 @default.
• W2012532921 hasConcept C153911025 @default.
• W2012532921 hasConcept C170493617 @default.
• W2012532921 hasConcept C173396325 @default.
• W2012532921 hasConcept C185592680 @default.
• W2012532921 hasConcept C190232843 @default.
• W2012532921 hasConcept C2776719180 @default.
• W2012532921 hasConcept C2780394083 @default.
• W2012532921 hasConcept C49039625 @default.
• W2012532921 hasConcept C502942594 @default.
• W2012532921 hasConcept C54009773 @default.

• next