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10.1186/s13046-016-0317-z http://scihub22266oqcxt.onion/10.1186/s13046-016-0317-z C4791758!4791758!26975989     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Exp+Clin+Cancer+Res 2016 ; 35 (ä): ä Nephropedia Template TP {{tp|p=26975989|t=2016. Pancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting |pdf=|usr=}}{{26975989}} gab.com Text Pancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting JO: J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26975989 #FOAvip Background: Progressive loss of skeletal muscle, termed muscle wasting, is a hallmark of cancer cachexia and contributes to weakness, reduced quality of life, as well as poor response to therapy. Previous studies have indicated that systemic host inflammatory response regarding tumor development results in muscle wasting. However, how tumor directly regulates muscle wasting via tumor-derived secreted proteins is still largely unknown. Methods: In this study, we performed bioinformatics analysis in two datasets of pancreatic ductal adenocarcinoma, which causes cancer cachexia and muscle wasting with the highest prevalence, and uncovered that IGFBP3, which encodes IGF-binding protein-3 (IGFBP-3), is dramatically up-regulated in pancreatic tumor samples. We also verified the wasting effect of IGFBP-3 on C2C12 muscle cells with biochemical and genetic assays. Results: IGFBP-3 potently leads to impaired myogenesis and enhanced muscle protein degradation, the major features of muscle wasting, via IGF signaling inhibition. Moreover, conditioned medium from Capan-1 pancreatic cancer cells, which contains abundant IGFBP-3, significantly induces muscle cell wasting. This wasting effect is potently alleviated by IGFBP3 knockdown in Capan-1 cells or IGFBP-3 antibody neutralization. Strikingly, compared to muscle cells, IGF signaling and proliferation rate of Capan-1 cells were rarely affected by IGFBP-3 treatment. Conclusions: Our results demonstrated that pancreatic cancer cells induce muscle wasting via IGFBP-3 production. Electronic supplementary material: The online version of this article (doi:10.1186/s13046-016-0317-z) contains supplementary material, which is available to authorized users. Twit Text FOAVip Pancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting ????J Exp Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26975989 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26975989 #FOAvip English Wikipedia <ref>{{Cite pmid|26975989}}</ref> Pancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting #MMPMID26975989 Huang Xy; Huang Zl; Yang Jh; Xu Yh; Sun JS; Zheng Q; Wei C; Song W; Yuan Z J Exp Clin Cancer Res 2016[]; 35 (ä): ä PMID26975989show ga Background: Progressive loss of skeletal muscle, termed muscle wasting, is a hallmark of cancer cachexia and contributes to weakness, reduced quality of life, as well as poor response to therapy. Previous studies have indicated that systemic host inflammatory response regarding tumor development results in muscle wasting. However, how tumor directly regulates muscle wasting via tumor-derived secreted proteins is still largely unknown. Methods: In this study, we performed bioinformatics analysis in two datasets of pancreatic ductal adenocarcinoma, which causes cancer cachexia and muscle wasting with the highest prevalence, and uncovered that IGFBP3, which encodes IGF-binding protein-3 (IGFBP-3), is dramatically up-regulated in pancreatic tumor samples. We also verified the wasting effect of IGFBP-3 on C2C12 muscle cells with biochemical and genetic assays. Results: IGFBP-3 potently leads to impaired myogenesis and enhanced muscle protein degradation, the major features of muscle wasting, via IGF signaling inhibition. Moreover, conditioned medium from Capan-1 pancreatic cancer cells, which contains abundant IGFBP-3, significantly induces muscle cell wasting. This wasting effect is potently alleviated by IGFBP3 knockdown in Capan-1 cells or IGFBP-3 antibody neutralization. Strikingly, compared to muscle cells, IGF signaling and proliferation rate of Capan-1 cells were rarely affected by IGFBP-3 treatment. Conclusions: Our results demonstrated that pancreatic cancer cells induce muscle wasting via IGFBP-3 production. Electronic supplementary material: The online version of this article (doi:10.1186/s13046-016-0317-z) contains supplementary material, which is available to authorized users. äPancreatic cancer cell-derived IGFBP-3 contributes to muscle wasting (epmc).pdf DeepDyve Pubget Overpricing