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10.1038/srep27886 http://scihub22266oqcxt.onion/10.1038/srep27886 C4904223!4904223 !27292568     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27292568 &cmd=llinks): Failed to open stream: HTTP request failed! 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The Novel Antitubulin Agent TR-764 Strongly Reduces Tumor Vasculature and Inhibits HIF-1? Activation |pdf=|usr=}}{{27292568 }} gab.com Text The Novel Antitubulin Agent TR-764 Strongly Reduces Tumor Vasculature and Inhibits HIF-1 Activation JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27292568 #FOAvip Tubulin binding agents (TBAs) are commonly used in cancer therapy as antimitotics. It has been described that TBAs, like combretastatin A-4 (CA-4), present also antivascular activity and among its derivatives we identified TR-764 as a new inhibitor of tubulin polymerization, based on the 2-(alkoxycarbonyl)-3-(3',4',5'-trimethoxyanilino)benzo[b]thiophene molecular skeleton. The antiangiogenic activity of TR-764 (1-10?nM) was tested in vitro on human umbilical endothelial cells (HUVECs), and in vivo, on the chick embryo chorioallantoic membrane (CAM) and two murine tumor models. TR-764 binding to tubulin triggers cytoskeleton rearrangement without affecting cell cycle and viability. It leads to capillary tube disruption, increased cell permeability, and cell motility reduction. Moreover it disrupts adherens junctions and focal adhesions, through mechanisms involving VE-cadherin/?-catenin and FAK/Src. Importantly, TR-764 is active in hypoxic conditions significantly reducing HIF-1?. In vivo TR-764 (1-100?pmol/egg) remarkably blocks the bFGF proangiogenic activity on CAM and shows a stronger reduction of tumor mass and microvascular density both in murine syngeneic and xenograft tumor models, compared to the lead compound CA-4P. Altogether, our results indicate that TR-764 is a novel TBA with strong potential as both antivascular and antitumor molecule that could improve the common anticancer therapies, by overcoming hypoxia-induced resistance mechanisms. Twit Text FOAVip The Novel Antitubulin Agent TR-764 Strongly Reduces Tumor Vasculature and Inhibits HIF-1 Activation ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27292568 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27292568 #FOAvip English Wikipedia <ref>{{Cite pmid|27292568 }}</ref> The Novel Antitubulin Agent TR-764 Strongly Reduces Tumor Vasculature and Inhibits HIF-1? Activation #MMPMID27292568 Porcù E ; Persano L ; Ronca R ; Mitola S ; Bortolozzi R ; Romagnoli R ; Oliva P ; Basso G ; Viola G Sci Rep 2016[Jun]; 6 (ä): 27886 PMID27292568 show ga Tubulin binding agents (TBAs) are commonly used in cancer therapy as antimitotics. It has been described that TBAs, like combretastatin A-4 (CA-4), present also antivascular activity and among its derivatives we identified TR-764 as a new inhibitor of tubulin polymerization, based on the 2-(alkoxycarbonyl)-3-(3',4',5'-trimethoxyanilino)benzo[b]thiophene molecular skeleton. The antiangiogenic activity of TR-764 (1-10?nM) was tested in vitro on human umbilical endothelial cells (HUVECs), and in vivo, on the chick embryo chorioallantoic membrane (CAM) and two murine tumor models. TR-764 binding to tubulin triggers cytoskeleton rearrangement without affecting cell cycle and viability. It leads to capillary tube disruption, increased cell permeability, and cell motility reduction. Moreover it disrupts adherens junctions and focal adhesions, through mechanisms involving VE-cadherin/?-catenin and FAK/Src. Importantly, TR-764 is active in hypoxic conditions significantly reducing HIF-1?. In vivo TR-764 (1-100?pmol/egg) remarkably blocks the bFGF proangiogenic activity on CAM and shows a stronger reduction of tumor mass and microvascular density both in murine syngeneic and xenograft tumor models, compared to the lead compound CA-4P. Altogether, our results indicate that TR-764 is a novel TBA with strong potential as both antivascular and antitumor molecule that could improve the common anticancer therapies, by overcoming hypoxia-induced resistance mechanisms. |Actin Cytoskeleton/*drug effects [MESH] |Aniline Compounds/*pharmacology [MESH] |Animals [MESH] |Antigens, CD/metabolism [MESH] |Cadherins/metabolism [MESH] |Cell Adhesion/drug effects [MESH] |Cell Membrane Permeability/drug effects [MESH] |Cell Movement/drug effects [MESH] |Chick Embryo [MESH] |Chickens [MESH] |Chorioallantoic Membrane/blood supply/drug effects [MESH] |Fibroblast Growth Factors/pharmacology [MESH] |Human Umbilical Vein Endothelial Cells [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Neoplasms/drug therapy/pathology [MESH] |Neovascularization, Physiologic/drug effects [MESH] |Stilbenes/therapeutic use/toxicity [MESH] |Thiophenes/*pharmacology [MESH] |Tubulin Modulators/chemistry/therapeutic use/*toxicity [MESH] |Vascular Endothelial Growth Factor A/pharmacology [MESH]The Novel Antitubulin Agent TR-764 Strongly Reduces Tumor Vasculature (epmc).pdf DeepDyve Pubget Overpricing