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10.1038/ncomms7285 http://scihub22266oqcxt.onion/10.1038/ncomms7285 C4366489!4366489!25734337     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun ä ; 6 (ä): ä Nephropedia Template TP {{tp|p=25734337|t=ä. Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis |pdf=|usr=}}{{25734337}} gab.com Text Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25734337 #FOAvip STAT3 is considered to play an oncogenic role in several malignancies including lung cancer; consequently, targeting STAT3 is currently proposed as therapeutic intervention. Here we demonstrate that STAT3 plays an unexpected tumour-suppressive role in KRAS mutant lung adenocarcinoma (AC). Indeed, lung tissue-specific inactivation of Stat3 in mice results in increased KrasG12D-driven AC initiation and malignant progression leading to markedly reduced survival. Knockdown of STAT3 in xenografted human AC cells increases tumour growth. Clinically, low STAT3 expression levels correlate with poor survival and advanced malignancy in human lung AC patients with smoking history, which are prone to KRAS mutations. Consistently, KRAS mutant lung tumours exhibit reduced STAT3 levels. Mechanistically, we demonstrate that STAT3 controls NF-?B-induced IL-8 expression by sequestering NF-?B within the cytoplasm, thereby inhibiting IL-8-mediated myeloid tumour infiltration and tumour vascularization and hence tumour progression. These results elucidate a novel STAT3?NF-?B?IL-8 axis in KRAS mutant AC with therapeutic and prognostic relevance. Twit Text FOAVip Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25734337 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25734337 #FOAvip English Wikipedia <ref>{{Cite pmid|25734337}}</ref> Disruption of STAT3 signalling promotes KRAS-induced lung tumorigenesis #MMPMID25734337 Grabner B; Schramek D; Mueller KM; Moll HP; Svinka J; Hoffmann T; Bauer E; Blaas L; Hruschka N; Zboray K; Stiedl P; Nivarthi H; Bogner E; Gruber W; Mohr T; Zwick RH; Kenner L; Poli V; Aberger F; Stoiber D; Egger G; Esterbauer H; Zuber J; Moriggl R; Eferl R; Gy?rffy B; Penninger JM; Popper H; Casanova E Nat Commun ä[]; 6 (ä): ä PMID25734337show ga STAT3 is considered to play an oncogenic role in several malignancies including lung cancer; consequently, targeting STAT3 is currently proposed as therapeutic intervention. Here we demonstrate that STAT3 plays an unexpected tumour-suppressive role in KRAS mutant lung adenocarcinoma (AC). Indeed, lung tissue-specific inactivation of Stat3 in mice results in increased KrasG12D-driven AC initiation and malignant progression leading to markedly reduced survival. Knockdown of STAT3 in xenografted human AC cells increases tumour growth. Clinically, low STAT3 expression levels correlate with poor survival and advanced malignancy in human lung AC patients with smoking history, which are prone to KRAS mutations. Consistently, KRAS mutant lung tumours exhibit reduced STAT3 levels. Mechanistically, we demonstrate that STAT3 controls NF-?B-induced IL-8 expression by sequestering NF-?B within the cytoplasm, thereby inhibiting IL-8-mediated myeloid tumour infiltration and tumour vascularization and hence tumour progression. These results elucidate a novel STAT3?NF-?B?IL-8 axis in KRAS mutant AC with therapeutic and prognostic relevance. äDisruption of STAT3 signalling promotes KRAS-induced lung tumorigenesi(epmc).pdf DeepDyve Pubget Overpricing