{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fernandez-Marcos PJ"],"funding":["NIAID NIH HHS"],"pagination":["12962-7"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2722271"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["106(31)"],"pubmed_abstract":["Prostate cancer is one of the most common neoplasias in men. The tumor suppressor Par-4 is an important negative regulator of the canonical NF-kappaB pathway and is highly expressed in prostate. Here we show that Par-4 expression is lost in a high percentage of human prostate carcinomas, and this occurs in association with phosphatase and tensin homolog deleted from chromosome 10 (PTEN) loss. Par-4 null mice, similar to PTEN-heterozygous mice, only develop benign prostate lesions, but, importantly, concomitant Par-4 ablation and PTEN-heterozygosity lead to invasive prostate carcinoma in mice. This strong tumorigenic cooperation is anticipated in the preneoplastic prostate epithelium by an additive increase in Akt activation and a synergistic stimulation of NF-kappaB. These results establis"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Simultaneous inactivation of Par-4 and PTEN in vivo leads to synergistic NF-kappaB activation and invasive prostate carcinoma."],"pmcid":["PMC2722271"],"funding_grant_id":["R01 AI072581","R01-AI072581"],"pubmed_authors":["Moscat J","Joshi J","Castilla EA","Abu-Baker S","Saez C","Collado M","Palacios J","Galvez A","Moreno-Bueno G","Fernandez-Marcos PJ","Diaz-Meco MT","Canamero M","Leitges M","Serrano M"],"additional_accession":[]},"is_claimable":false,"name":"Simultaneous inactivation of Par-4 and PTEN in vivo leads to synergistic NF-kappaB activation and invasive prostate carcinoma.","description":"Prostate cancer is one of the most common neoplasias in men. The tumor suppressor Par-4 is an important negative regulator of the canonical NF-kappaB pathway and is highly expressed in prostate. Here we show that Par-4 expression is lost in a high percentage of human prostate carcinomas, and this occurs in association with phosphatase and tensin homolog deleted from chromosome 10 (PTEN) loss. Par-4 null mice, similar to PTEN-heterozygous mice, only develop benign prostate lesions, but, importantly, concomitant Par-4 ablation and PTEN-heterozygosity lead to invasive prostate carcinoma in mice. This strong tumorigenic cooperation is anticipated in the preneoplastic prostate epithelium by an additive increase in Akt activation and a synergistic stimulation of NF-kappaB. These results establis","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Aug","modification":"2025-04-05T15:10:10.129Z","creation":"2019-03-27T00:24:02Z"},"accession":"S-EPMC2722271","cross_references":{"pubmed":["19470463"],"doi":["10.1073/pnas.0813055106"]}}