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10.1002/1878-0261.12089 http://scihub22266oqcxt.onion/10.1002/1878-0261.12089 C5579338!5579338!28580735     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Oncol 2017 ; 11 (9): 1208-24 Nephropedia Template TP {{tp|p=28580735|t=2017. DDAH1 mediates gastric cancer cell invasion and metastasis via Wnt/??catenin signaling pathway |pdf=|usr=}}{{28580735}} gab.com Text DDAH1 mediates gastric cancer cell invasion and metastasis via Wnt/ catenin signaling pathway JO: Mol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28580735 #FOAvip Gastric cancer (GC) represents the fourth most common malignant neoplasm and the second leading cause of cancer death. Despite therapeutic advances in recent decades, the clinical outcome remains dismal owing to the fact that most patients with GC show advanced disease at diagnosis and current chemotherapy only confers a modest survival advantage. Identification of key molecular signaling pathways involved in gastric carcinogenesis and progression would aid in early diagnosis and provide a rational design for targeted therapies in selected patients with advanced GC, to improve their outcome. Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is the main enzyme that can degrade asymmetric dimethylarginine, an endogenous nitric oxide synthase (NOS) inhibitor. Increased DDAH1 expression and NO production have been linked to multiple pathological conditions including cancer. However, the prognostic significance of DDAH1 in patients with GC and its function in GC progression remain undefined. In this study, we found that downregulation of DDAH1 was frequently detected in GC tissues and strongly correlated with more aggressive phenotypes and poor prognosis. Functional assays confirmed that forced expression of DDAH1 in the GC cells suppressed cell migration and invasion in vitro, as well as metastatic potential in vivo. DDAH1 overexpression inhibited the epithelial?mesenchymal transition process by increasing ??catenin degradation through the attenuation of Wnt/GSK?3? signaling. In contrast, knockdown of DDAH1 produced the opposite effect. These findings suggest that DDAH1 functions as a tumor suppressor in GC and may be exploited as a diagnostic and prognostic biomarker for GC. Twit Text FOAVip DDAH1 mediates gastric cancer cell invasion and metastasis via Wnt/ catenin signaling pathway ????Mol Oncol http://www.kidney.de/pget.php?&tw=1&pmid=28580735 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28580735 #FOAvip English Wikipedia <ref>{{Cite pmid|28580735}}</ref> DDAH1 mediates gastric cancer cell invasion and metastasis via Wnt/??catenin signaling pathway #MMPMID28580735 Ye J; Xu J; Li Y; Huang Q; Huang J; Wang J; Zhong W; Lin X; Chen W; Lin X Mol Oncol 2017[Sep]; 11 (9): 1208-24 PMID28580735show ga Gastric cancer (GC) represents the fourth most common malignant neoplasm and the second leading cause of cancer death. Despite therapeutic advances in recent decades, the clinical outcome remains dismal owing to the fact that most patients with GC show advanced disease at diagnosis and current chemotherapy only confers a modest survival advantage. Identification of key molecular signaling pathways involved in gastric carcinogenesis and progression would aid in early diagnosis and provide a rational design for targeted therapies in selected patients with advanced GC, to improve their outcome. Dimethylarginine dimethylaminohydrolase 1 (DDAH1) is the main enzyme that can degrade asymmetric dimethylarginine, an endogenous nitric oxide synthase (NOS) inhibitor. Increased DDAH1 expression and NO production have been linked to multiple pathological conditions including cancer. However, the prognostic significance of DDAH1 in patients with GC and its function in GC progression remain undefined. In this study, we found that downregulation of DDAH1 was frequently detected in GC tissues and strongly correlated with more aggressive phenotypes and poor prognosis. Functional assays confirmed that forced expression of DDAH1 in the GC cells suppressed cell migration and invasion in vitro, as well as metastatic potential in vivo. DDAH1 overexpression inhibited the epithelial?mesenchymal transition process by increasing ??catenin degradation through the attenuation of Wnt/GSK?3? signaling. In contrast, knockdown of DDAH1 produced the opposite effect. These findings suggest that DDAH1 functions as a tumor suppressor in GC and may be exploited as a diagnostic and prognostic biomarker for GC. äDDAH1 mediates gastric cancer cell invasion and metastasis via Wnt/??c(epmc).pdf DeepDyve Pubget Overpricing