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10.1124/mol.114.096941 http://scihub22266oqcxt.onion/10.1124/mol.114.096941 C4419284!4419284!25552486     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Pharmacol 2015 ; 87 (3): 501-12 Nephropedia Template TP {{tp|p=25552486|t=2015. Repurposing the Antipsychotic Trifluoperazine as an Antimetastasis Agent |pdf=|usr=}}{{25552486}} gab.com Text Repurposing the Antipsychotic Trifluoperazine as an Antimetastasis Agent JO: Mol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=25552486 #FOAvip Because cancer cell invasion is a critical determinant of metastasis, targeting invasion is a viable approach to prevent metastasis. Utilizing a novel three-dimensional high-throughput invasion assay, we screened a National Cancer Institute compound library and discovered compounds demonstrating inhibitory effects on cancer cell invasion. One hit, trifluoperazine, suppresses invasion of human cancer cell lines while displaying a limited cytotoxicity profile. This inhibition is due to the interference with cancer cell migratory ability but not proteolytic activity. Treatment of cancer cells with trifluoperazine significantly reduces angiogenesis and prevents cancer cell invasion through a chorioallantoic basement membrane. Mechanistically, treatment results in decreased phosphorylated AKT (Ser473 and Thr308) and ?-catenin (Ser552). Lack of phosphorylation of Ser552 of ?-catenin prevents ?-catenin nuclear relocation, resulting in decreased expression of vascular endothelial growth factor, likely mediated through dopamine receptor D2. Taken together, we demonstrated that trifluoperazine is responsible for reducing the angiogenic and invasive potential of aggressive cancer cells through dopamine receptor D2 to modulate the ?-catenin pathway and propose that trifluoperazine may be used as an antimetastasis chemotherapeutic. Twit Text FOAVip Repurposing the Antipsychotic Trifluoperazine as an Antimetastasis Agent ????Mol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=25552486 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25552486 #FOAvip English Wikipedia <ref>{{Cite pmid|25552486}}</ref> Repurposing the Antipsychotic Trifluoperazine as an Antimetastasis Agent #MMPMID25552486 Pulkoski-Gross A; Li J; Zheng C; Li Y; Ouyang N; Rigas B; Zucker S; Cao J Mol Pharmacol 2015[Mar]; 87 (3): 501-12 PMID25552486show ga Because cancer cell invasion is a critical determinant of metastasis, targeting invasion is a viable approach to prevent metastasis. Utilizing a novel three-dimensional high-throughput invasion assay, we screened a National Cancer Institute compound library and discovered compounds demonstrating inhibitory effects on cancer cell invasion. One hit, trifluoperazine, suppresses invasion of human cancer cell lines while displaying a limited cytotoxicity profile. This inhibition is due to the interference with cancer cell migratory ability but not proteolytic activity. Treatment of cancer cells with trifluoperazine significantly reduces angiogenesis and prevents cancer cell invasion through a chorioallantoic basement membrane. Mechanistically, treatment results in decreased phosphorylated AKT (Ser473 and Thr308) and ?-catenin (Ser552). Lack of phosphorylation of Ser552 of ?-catenin prevents ?-catenin nuclear relocation, resulting in decreased expression of vascular endothelial growth factor, likely mediated through dopamine receptor D2. Taken together, we demonstrated that trifluoperazine is responsible for reducing the angiogenic and invasive potential of aggressive cancer cells through dopamine receptor D2 to modulate the ?-catenin pathway and propose that trifluoperazine may be used as an antimetastasis chemotherapeutic. äRepurposing the Antipsychotic Trifluoperazine as an Antimetastasis Age(epmc).pdf DeepDyve Pubget Overpricing