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10.1111/cas.13138 http://scihub22266oqcxt.onion/10.1111/cas.13138 C5378285!5378285 !28002618     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28002618 &cmd=llinks): Failed to open stream: HTTP request failed! 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Verteporfin suppresses cell survival, angiogenesis and vasculogenic mimicry of pancreatic ductal adenocarcinoma via disrupting the YAP-TEAD complex |pdf=|usr=}}{{28002618 }} gab.com Text Verteporfin suppresses cell survival, angiogenesis and vasculogenic mimicry of pancreatic ductal adenocarcinoma via disrupting the YAP-TEAD complex JO: Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28002618 #FOAvip Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive human malignancies. The Yes-associated protein-1 (YAP) plays a critical role in cell proliferation, apoptosis and angiogenesis. Verteporfin is a photosensitizer used in photodynamic therapy and also a small molecular inhibitor of the Hippo-YAP pathway. However, little is known about whether verteporfin could inhibit YAP activity in PDAC cells. Our present results showed that verteporfin suppressed the proliferation of human PDAC PANC-1 and SW1990 cells by arresting cells at the G1 phase, and inducing apoptosis in dose- and time-dependent manners. Verteporfin also inhibited the tumor growth on the PDAC xenograft model. Treatment with verteporfin led to downregulation of cyclinD1 and cyclinE1, modulation of Bcl-2 family proteins and activation of PARP. In addition, verteporfin exhibited an inhibitory effect on angiogenesis and vasculogenic mimicry via suppressing Ang2, MMP2, VE-cadherin, and ?-SMA expression in vitro and in vivo. Mechanism studies demonstrated that verteporfin impaired YAP and TEAD interaction to suppress the expression of targeted genes. Our results provide a foundation for repurposing verteporfin as a promising anti-tumor drug in the treatment of pancreatic cancer by targeting the Hippo pathway. Twit Text FOAVip Verteporfin suppresses cell survival, angiogenesis and vasculogenic mimicry of pancreatic ductal adenocarcinoma via disrupting the YAP-TEAD complex ????Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28002618 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28002618 #FOAvip English Wikipedia <ref>{{Cite pmid|28002618 }}</ref> Verteporfin suppresses cell survival, angiogenesis and vasculogenic mimicry of pancreatic ductal adenocarcinoma via disrupting the YAP-TEAD complex #MMPMID28002618 Wei H ; Wang F ; Wang Y ; Li T ; Xiu P ; Zhong J ; Sun X ; Li J Cancer Sci 2017[Mar]; 108 (3 ): 478-487 PMID28002618 show ga Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive human malignancies. The Yes-associated protein-1 (YAP) plays a critical role in cell proliferation, apoptosis and angiogenesis. Verteporfin is a photosensitizer used in photodynamic therapy and also a small molecular inhibitor of the Hippo-YAP pathway. However, little is known about whether verteporfin could inhibit YAP activity in PDAC cells. Our present results showed that verteporfin suppressed the proliferation of human PDAC PANC-1 and SW1990 cells by arresting cells at the G1 phase, and inducing apoptosis in dose- and time-dependent manners. Verteporfin also inhibited the tumor growth on the PDAC xenograft model. Treatment with verteporfin led to downregulation of cyclinD1 and cyclinE1, modulation of Bcl-2 family proteins and activation of PARP. In addition, verteporfin exhibited an inhibitory effect on angiogenesis and vasculogenic mimicry via suppressing Ang2, MMP2, VE-cadherin, and ?-SMA expression in vitro and in vivo. Mechanism studies demonstrated that verteporfin impaired YAP and TEAD interaction to suppress the expression of targeted genes. Our results provide a foundation for repurposing verteporfin as a promising anti-tumor drug in the treatment of pancreatic cancer by targeting the Hippo pathway. |Adaptor Proteins, Signal Transducing/*antagonists & inhibitors/metabolism [MESH] |Animals [MESH] |Antigens, CD [MESH] |Antineoplastic Agents/*pharmacology [MESH] |Apoptosis/*drug effects [MESH] |Cadherins/antagonists & inhibitors [MESH] |Carcinoma, Pancreatic Ductal/drug therapy/*pathology [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cell Survival/drug effects [MESH] |Cyclin D1/metabolism [MESH] |Cyclin E/metabolism [MESH] |DNA-Binding Proteins/*antagonists & inhibitors/metabolism [MESH] |G1 Phase Cell Cycle Checkpoints/drug effects [MESH] |Human Umbilical Vein Endothelial Cells [MESH] |Humans [MESH] |Male [MESH] |Matrix Metalloproteinase 2/metabolism [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Nude [MESH] |Neovascularization, Pathologic/*drug therapy [MESH] |Nuclear Proteins/*antagonists & inhibitors/metabolism [MESH] |Oncogene Proteins/metabolism [MESH] |Pancreatic Neoplasms/drug therapy/*pathology [MESH] |Phosphoproteins/*antagonists & inhibitors/metabolism [MESH] |Poly (ADP-Ribose) Polymerase-1/metabolism [MESH] |Porphyrins/*pharmacology [MESH] |Proto-Oncogene Proteins c-bcl-2/metabolism [MESH] |TEA Domain Transcription Factors [MESH] |Transcription Factors/*antagonists & inhibitors/metabolism [MESH] |Verteporfin [MESH] |Vesicular Transport Proteins/antagonists & inhibitors [MESH] |Xenograft Model Antitumor Assays [MESH]Verteporfin suppresses cell survival, angiogenesis and vasculogenic mi(epmc).pdf DeepDyve Pubget Overpricing