Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1136/gutjnl-2016-312278 http://scihub22266oqcxt.onion/10.1136/gutjnl-2016-312278 C5530482!5530482!27618837     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Gut 2017 ; 66 (7): 1268-77 Nephropedia Template TP {{tp|p=27618837|t=2017. Wnt signalling modulates transcribed-ultraconserved regions in hepatobiliary cancers |pdf=|usr=}}{{27618837}} gab.com Text Wnt signalling modulates transcribed-ultraconserved regions in hepatobiliary cancers JO: Gut http://www.kidney.de/pget.php?&tw=1&pmid=27618837 #FOAvip Objective: Transcribed-ultraconserved regions (T-UCR) are long non-coding RNAs which are conserved across species and are involved in carcinogenesis. We studied T-UCRs downstream of the Wnt/?-catenin pathway in liver cancer. Design: Hypomorphic Apc mice (Apcfl/fl) and thiocetamide (TAA)-treated rats developed Wnt/?-catenin dependent hepatocarcinoma (HCC) and cholangiocarcinoma (CCA), respectively. T-UCR expression was assessed by microarray, real-time PCR and in situ hybridisation. Results: Overexpression of the T-UCR uc.158? could differentiate Wnt/?-catenin dependent HCC from normal liver and from ?-catenin negative diethylnitrosamine (DEN)-induced HCC. uc.158? was overexpressed in human HepG2 versus Huh7 cells in line with activation of the Wnt pathway. In vitro modulation of ?-catenin altered uc.158? expression in human malignant hepatocytes. uc.158? expression was increased in CTNNB1-mutated human HCCs compared with non-mutated human HCCs, and in human HCC with nuclear localisation of ?-catenin. uc.158? was increased in TAA rat CCA and reduced after treatment with Wnt/?-catenin inhibitors. uc.158? expression was negative in human normal liver and biliary epithelia, while it was increased in human CCA in two different cohorts. Locked nucleic acid-mediated inhibition of uc.158? reduced anchorage cell growth, 3D-spheroid formation and spheroid-based cell migration, and increased apoptosis in HepG2 and SW1 cells. miR-193b was predicted to have binding sites within the uc.158? sequence. Modulation of uc.158? changed miR-193b expression in human malignant hepatocytes. Co-transfection of uc.158? inhibitor and anti-miR-193b rescued the effect of uc.158? inhibition on cell viability. Conclusions: We showed that uc.158? is activated by the Wnt pathway in liver cancers and drives their growth. Thus, it may represent a promising target for the development of novel therapeutics. Twit Text FOAVip Wnt signalling modulates transcribed-ultraconserved regions in hepatobiliary cancers ????Gut http://www.kidney.de/pget.php?&tw=1&pmid=27618837 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27618837 #FOAvip English Wikipedia <ref>{{Cite pmid|27618837}}</ref> Wnt signalling modulates transcribed-ultraconserved regions in hepatobiliary cancers #MMPMID27618837 Carotenuto P; Fassan M; Pandolfo R; Lampis A; Vicentini C; Cascione L; Paulus-Hock V; Boulter L; Guest R; Quagliata L; Hahne JC; Ridgway R; Jamieson T; Athineos D; Veronese A; Visone R; Murgia C; Ferrari G; Guzzardo V; Evans TRJ; MacLeod M; Feng GJ; Dale T; Negrini M; Forbes SJ; Terracciano L; Scarpa A; Patel T; Valeri N; Workman P; Sansom O; Braconi C Gut 2017[Jul]; 66 (7): 1268-77 PMID27618837show ga Objective: Transcribed-ultraconserved regions (T-UCR) are long non-coding RNAs which are conserved across species and are involved in carcinogenesis. We studied T-UCRs downstream of the Wnt/?-catenin pathway in liver cancer. Design: Hypomorphic Apc mice (Apcfl/fl) and thiocetamide (TAA)-treated rats developed Wnt/?-catenin dependent hepatocarcinoma (HCC) and cholangiocarcinoma (CCA), respectively. T-UCR expression was assessed by microarray, real-time PCR and in situ hybridisation. Results: Overexpression of the T-UCR uc.158? could differentiate Wnt/?-catenin dependent HCC from normal liver and from ?-catenin negative diethylnitrosamine (DEN)-induced HCC. uc.158? was overexpressed in human HepG2 versus Huh7 cells in line with activation of the Wnt pathway. In vitro modulation of ?-catenin altered uc.158? expression in human malignant hepatocytes. uc.158? expression was increased in CTNNB1-mutated human HCCs compared with non-mutated human HCCs, and in human HCC with nuclear localisation of ?-catenin. uc.158? was increased in TAA rat CCA and reduced after treatment with Wnt/?-catenin inhibitors. uc.158? expression was negative in human normal liver and biliary epithelia, while it was increased in human CCA in two different cohorts. Locked nucleic acid-mediated inhibition of uc.158? reduced anchorage cell growth, 3D-spheroid formation and spheroid-based cell migration, and increased apoptosis in HepG2 and SW1 cells. miR-193b was predicted to have binding sites within the uc.158? sequence. Modulation of uc.158? changed miR-193b expression in human malignant hepatocytes. Co-transfection of uc.158? inhibitor and anti-miR-193b rescued the effect of uc.158? inhibition on cell viability. Conclusions: We showed that uc.158? is activated by the Wnt pathway in liver cancers and drives their growth. Thus, it may represent a promising target for the development of novel therapeutics. äWnt signalling modulates transcribed-ultraconserved regions in hepatob(epmc).pdf DeepDyve Pubget Overpricing