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• W2623082743 abstract "// Lu-Lu Wang 1 , Lan-Bo Zhou 2 , Jin Shu 3 , Nan-Nan Li 1 , Hui-Wen Zhang 1 , Rui Jin 1 , Li-Li Zhuang 1 and Guo-Ping Zhou 1 1 Department of Pediatrics, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China 2 Grade 2013 Clinical Class 7, The First School of Clinical Medicine, Nanjing Medical University, Nanjing, Jiangsu Province, China 3 Department of Pediatric Respiration, Affiliated Wuxi People’s Hospital, Nanjing Medical University, Wuxi, Jiangsu, China Correspondence to: Guo-Ping Zhou, email: guopingzhou@aliyun.com Keywords: interferon regulatroy factor 3, GATA-1, acetylation, histone deacetylase inhibitor, lung adenocarcinoma Received: December 20, 2016      Accepted: April 21, 2017      Published: June 06, 2017 ABSTRACT Interferon regulatory factor 3 (IRF-3) is an important transcription factor for interferon genes. Although its functional activation by viral infection has been widely explicated, the regulatory mechanism of IRF-3 gene expression in cancer cells is poorly understood. In this study, we demonstrated treatment of lung adenocarcinoma A549 cells with trichostatin A (TSA) and valproic acid (VPA), two different classes of histone deacetylase inhibitors, strongly stimulated IRF-3 gene expression. Truncated and mutated IRF-3 promoter indicated that a specific GATA-1 element was responsible for TSA-induced activation of IRF-3 promoter. Chromatin immunoprecipitation and electrophoretic mobility shift assay showed that TSA treatment increased the binding affinity of GATA-1 to IRF-3 promoter. Using immunoprecipitation assay and immunoblotting, we demonstrated that TSA increased the level of acetylated GATA-1 in A549 cells. In summary, our study implied that TSA enhanced IRF-3 gene expression through increased GATA-1 recruitment to IRF-3 promoter and the acetylation level of GATA-1 in lung adenocarcinoma A549 cells." @default.
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• W2623082743 date "2017-06-06" @default.
• W2623082743 modified "2023-10-16" @default.
• W2623082743 title "Up-regulation of IRF-3 expression through GATA-1 acetylation by histone deacetylase inhibitor in lung adenocarcinoma A549 cells" @default.
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• W2623082743 doi "https://doi.org/10.18632/oncotarget.18371" @default.
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