Class I histone deacetylases regulate p53/NF-κB crosstalk in cancer cells

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• 作者：Claudia Sch&auml ; fer^a ; Anja Gö ; der^b ; Mandy Beyer^b ; Nicole Kiweler^b ; Nisintha Mahendrarajah^b ; Anke Rauch^a ; Teodora Nikolova^b ; Natasa Stojanovic^c ; Martin Wieczorek^a ; Thomas R. Reich^b ; Maja T. Tomicic^b ; Michael Linnebacher^d ; Jü ; rgen Sonnemann^e ; Sascha Dietrich^f ; Andreas Sellmer^g ; Siavosh Mahboobi^g ; Thorsten Heinzel^a ; Gü ; nter Schneider^h ; ¹ ; Oliver H. Kr&auml ; mer^b ; ¹ ; ^{okraemer@uni-mainz.de}
• 关键词：BCL ; B cell lymphoma ; CLL ; chronic lymphatic leukemia ; DSB ; DNA double strand break ; HDAC ; histone deacetylase ; HDACi ; histone deacetylase inhibitor ; MS-275 ; entinostat ; NF-κB ; nuclear factor &lsquo ; kappa-light-chain-enhancer&rsquo ; of activated B cells ; PDAC ; pancreatic ductal adenocarcinoma ; PTM ; posttranslational modification ; VPA ; valproic acid
• 刊名：Cellular Signalling
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：29
• 期：Complete
• 页码：218-225
• 全文大小：1374 K
• 卷排序：29

文摘

Chemotherapeutic drugs induce NF-κB/p53 crosstalk in cell lines and primary cells. HDACi antagonize p53-dependent anti-apoptotic NF-κB-dependent gene expression. HDACi against class I HDACs reduce p53 levels in various tumor cells. Class I HDACi are necessary for the crosstalk between mutant p53 and NF-κB. Highly specific HDACi are tools to disclose biological functions of HDACs.