| Literature DB >> 25437558 |
Christopher S Hackett1, David A Quigley2, Robyn A Wong3, Justin Chen1, Christine Cheng3, Young K Song4, Jun S Wei4, Ludmila Pawlikowska5, Yun Bao3, David D Goldenberg3, Kim Nguyen3, W Clay Gustafson6, Sundari K Rallapalli7, Yoon-Jae Cho8, James M Cook7, Serguei Kozlov9, Jian-Hua Mao10, Terry Van Dyke9, Pui-Yan Kwok11, Javed Khan4, Allan Balmain2, QiWen Fan12, William A Weiss13.
Abstract
The development of targeted therapeutics for neuroblastoma, the third most common tumor in children, has been limited by a poor understanding of growth signaling mechanisms unique to the peripheral nerve precursors from which tumors arise. In this study, we combined genetics with gene-expression analysis in the peripheral sympathetic nervous system to implicate arginase 1 and GABA signaling in tumor formation in vivo. In human neuroblastoma cells, either blockade of ARG1 or benzodiazepine-mediated activation of GABA-A receptors induced apoptosis and inhibited mitogenic signaling through AKT and MAPK. These results suggest that ARG1 and GABA influence both neural development and neuroblastoma and that benzodiazepines in clinical use may have potential applications for neuroblastoma therapy.Entities:
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Year: 2014 PMID： 25437558 PMCID： PMC4251494 DOI： 10.1016/j.celrep.2014.09.046
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423