<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Huang,Guosheng</style></author><author><style face="normal" font="default" size="100%">Eisenberg,Rosana</style></author><author><style face="normal" font="default" size="100%">Yan,Min</style></author><author><style face="normal" font="default" size="100%">Monti,Stefano</style></author><author><style face="normal" font="default" size="100%">Lawrence,Earl</style></author><author><style face="normal" font="default" size="100%">Fu,Pingfu</style></author><author><style face="normal" font="default" size="100%">Walbroehl,Jaclyn</style></author><author><style face="normal" font="default" size="100%">L</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">15-Hydroxyprostaglandin dehydrogenase is a target of hepatocyte nuclear factor 3beta and a tumor suppressor in lung cancer</style></title><secondary-title><style face="normal" font="default" size="100%">Cancer Research</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adenocarcinoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Binding Sites</style></keyword><keyword><style  face="normal" font="default" size="100%">Cancer</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzymologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepatocyte Nuclear Factor 3-beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydroxyp</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Suppressor</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2008</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2008/07/01/</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/18593902</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">68</style></volume><pages><style face="normal" font="default" size="100%">5040 - 8</style></pages><isbn><style face="normal" font="default" size="100%">1538-7445</style></isbn><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The forkhead transcription factor hepatocyte nuclear factor 3beta (HNF3beta) is essential in foregut development and the regulation of lung-specific genes. HNF3beta expression leads to growth arrest and apoptosis in lung cancer cells and HNF3beta is a candidate tumor suppressor in lung cancer. In a transcriptional profiling study using a conditional cell line system, we now identify 15-PGDH as one of the major genes induced by HNF3beta expression. 15-PGDH is a critical metabolic enzyme of proliferative prostaglandins, an antagonist to cyclooxygenase-2 and a tumor suppressor in colon cancer. We confirmed the regulation of 15-PGDH expression by HNF3beta in a number of systems and showed direct binding of HNF3beta to 15-PGDH promoter elements. Western blotting of lung cancer cell lines and immunohistochemical examination of human lung cancer tissues found loss of 15-PGDH expression in approximately 65% of lung cancers. Further studies using in vitro cell-based assays and in vivo xenograft tumorigenesis assays showed a lack of in vitro but significant in vivo tumor suppressor activity of 15-PGDH via an antiangiogenic mechanism analogous to its role in colon cancer. In summary, we identify 15-PGDH as a direct downstream effector of HNF3beta and show that 15-PGDH acts as a tumor suppressor in lung cancer.</style></abstract><issue><style face="normal" font="default" size="100%">13</style></issue></record></records></xml>
