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10.1038/s41598-017-04626-4 http://scihub22266oqcxt.onion/10.1038/s41598-017-04626-4 C5495754!5495754 !28674429     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28674429 &cmd=llinks): Failed to open stream: HTTP request failed! 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Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway |pdf=|usr=}}{{28674429 }} gab.com Text Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28674429 #FOAvip In this study we have tested the efficacy of citrate therapy in various cancer models. We found that citrate administration inhibited A549 lung cancer growth and additional benefit accrued in combination with cisplatin. Interestingly, citrate regressed Ras-driven lung tumors. Further studies indicated that citrate induced tumor cell differentiation. Additionally, citrate treated tumor samples showed significantly higher infiltrating T-cells and increased blood levels of numerous cytokines. Moreover, we found that citrate inhibited IGF-1R phosphorylation. In vitro studies suggested that citrate treatment inhibited AKT phosphorylation, activated PTEN and increased expression of p-eIF2a. We also found that p-eIF2a was decreased when PTEN was depleted. These data suggest that citrate acts on the IGF-1R-AKT-PTEN-eIF2a pathway. Additionally, metabolic profiling suggested that both glycolysis and the tricarboxylic acid cycle were suppressed in a similar manner in vitro in tumor cells and in vivo but only in tumor tissue. We reproduced many of these observations in an inducible Her2/Neu-driven breast cancer model and in syngeneic pancreatic tumor (Pan02) xenografts. Our data suggests that citrate can inhibit tumor growth in diverse tumor types and via multiple mechanisms. Dietary supplementation with citrate may be beneficial as a cancer therapy. Twit Text FOAVip Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28674429 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28674429 #FOAvip English Wikipedia <ref>{{Cite pmid|28674429 }}</ref> Citrate Suppresses Tumor Growth in Multiple Models through Inhibition of Glycolysis, the Tricarboxylic Acid Cycle and the IGF-1R Pathway #MMPMID28674429 Ren JG ; Seth P ; Ye H ; Guo K ; Hanai JI ; Husain Z ; Sukhatme VP Sci Rep 2017[Jul]; 7 (1 ): 4537 PMID28674429 show ga In this study we have tested the efficacy of citrate therapy in various cancer models. We found that citrate administration inhibited A549 lung cancer growth and additional benefit accrued in combination with cisplatin. Interestingly, citrate regressed Ras-driven lung tumors. Further studies indicated that citrate induced tumor cell differentiation. Additionally, citrate treated tumor samples showed significantly higher infiltrating T-cells and increased blood levels of numerous cytokines. Moreover, we found that citrate inhibited IGF-1R phosphorylation. In vitro studies suggested that citrate treatment inhibited AKT phosphorylation, activated PTEN and increased expression of p-eIF2a. We also found that p-eIF2a was decreased when PTEN was depleted. These data suggest that citrate acts on the IGF-1R-AKT-PTEN-eIF2a pathway. Additionally, metabolic profiling suggested that both glycolysis and the tricarboxylic acid cycle were suppressed in a similar manner in vitro in tumor cells and in vivo but only in tumor tissue. We reproduced many of these observations in an inducible Her2/Neu-driven breast cancer model and in syngeneic pancreatic tumor (Pan02) xenografts. Our data suggests that citrate can inhibit tumor growth in diverse tumor types and via multiple mechanisms. Dietary supplementation with citrate may be beneficial as a cancer therapy. |*Citric Acid Cycle/drug effects [MESH] |*Models, Biological [MESH] |*Signal Transduction/drug effects [MESH] |Animals [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Cisplatin/pharmacology [MESH] |Citric Acid/*metabolism/pharmacology [MESH] |Cytokines/biosynthesis [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Glycolysis/drug effects [MESH] |Humans [MESH] |Inflammation Mediators/metabolism [MESH] |Leukocytes/metabolism/pathology [MESH] |Mice [MESH] |Receptor, IGF Type 1/*metabolism [MESH] |Xenograft Model Antitumor Assays [MESH]Citrate Suppresses Tumor Growth in Multiple Models through Inhibition (epmc).pdf DeepDyve Pubget Overpricing