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组蛋白去乙酰化酶抑制剂通过GATA-1乙酰化上调肺腺癌A549细胞中IRF-3的表达。

Up-regulation of IRF-3 expression through GATA-1 acetylation by histone deacetylase inhibitor in lung adenocarcinoma A549 cells.

作者信息

Wang Lu-Lu, Zhou Lan-Bo, Shu Jin, Li Nan-Nan, Zhang Hui-Wen, Jin Rui, Zhuang Li-Li, Zhou Guo-Ping

机构信息

Department of Pediatrics, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu Province, China.

Grade 2013 Clinical Class 7, The First School of Clinical Medicine, Nanjing Medical University, Nanjing, Jiangsu Province, China.

出版信息

Oncotarget. 2017 Jun 6;8(44):75943-75951. doi: 10.18632/oncotarget.18371. eCollection 2017 Sep 29.

DOI:10.18632/oncotarget.18371
PMID:29100282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5652676/
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.

摘要

干扰素调节因子3（IRF-3）是干扰素基因的重要转录因子。尽管其被病毒感染后的功能激活已得到广泛阐释，但癌细胞中IRF-3基因表达的调控机制仍知之甚少。在本研究中，我们证明用曲古抑菌素A（TSA）和丙戊酸（VPA）这两种不同类型的组蛋白去乙酰化酶抑制剂处理肺腺癌A549细胞，能强烈刺激IRF-3基因表达。截短和突变的IRF-3启动子表明，一个特定的GATA-1元件负责TSA诱导的IRF-3启动子激活。染色质免疫沉淀和电泳迁移率变动分析表明，TSA处理增加了GATA-1与IRF-3启动子的结合亲和力。通过免疫沉淀分析和免疫印迹，我们证明TSA增加了A549细胞中乙酰化GATA-1的水平。总之，我们的研究表明，TSA通过增加GATA-1与IRF-3启动子的结合以及肺腺癌A549细胞中GATA-1的乙酰化水平来增强IRF-3基因表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/b20cff5abae9/oncotarget-08-75943-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/15e5579485c2/oncotarget-08-75943-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/87db575833c8/oncotarget-08-75943-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/e4309fe4ad4e/oncotarget-08-75943-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/3cb6dc5207e8/oncotarget-08-75943-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/b20cff5abae9/oncotarget-08-75943-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/15e5579485c2/oncotarget-08-75943-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/87db575833c8/oncotarget-08-75943-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/e4309fe4ad4e/oncotarget-08-75943-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/3cb6dc5207e8/oncotarget-08-75943-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a53/5652676/b20cff5abae9/oncotarget-08-75943-g005.jpg

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