GATA3 acetylation at K119 by CBP inhibits cell migration and invasion in lung adenocarcinoma

GATA3 acetylation at K119 by CBP inhibits cell migration and invasion in lung adenocarcinoma
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CBP 对 GATA3 K119 的乙酰化可抑制肺腺癌中的细胞迁移和侵袭。

DOI:
10.1016/j.bbrc.2018.02.120
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发表时间:
2018-03-04
影响因子:
3.1
通讯作者:
Zhang, Hongquan
Zhang, Hongquan
中科院分区:
生物学4区
文献类型:
--
作者:
Li, Xueying;Jin, Jiaqi;Zhang, Hongquan

文献摘要

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GATA 3是一种参与多器官发育的转录因子。GATA 3的翻译后修饰对其功能至关重要。在这里,我们报告说,GATA 3相互作用,并乙酰化的乙酰转移酶CBP。I类脱乙酰酶HDAC 1、HDAC 2和HDAC 3使GATA 3脱乙酰。肺腺癌细胞中GATA 3的主要乙酰化位点被确定在赖氨酸119(AcK 119)。在功能上,GATA 3-乙酰化模拟K119 Q突变体被发现抑制肺腺癌细胞的迁移和侵袭,同时下调EMT控制转录因子Slug,Zeb 1和Zeb 2。综上所述,我们证明CBP在赖氨酸119处的GATA 3乙酰化阻碍了肺腺癌细胞的迁移和侵袭。(C)2018爱思唯尔公司All rights reserved.
GATA3 is a transcriptional factor involved in the development of multiple organs. Post translational modifications of GATA3 are critical to its function. Here, we report that GATA3 interacts with and is acetylated by the acetyltransferase CBP. Class I deacetylases HDAC1, HDAC2 and HDAC3 deacetylate GATA3. The major acetylated site of GATA3 in lung adenocarcinoma cells was determined at lysine 119 (AcK119). Functionally, GATA3-acetylation mimics K119Q mutant was found to inhibit lung adenocarcinoma cell migration and invasion with concomitant downregulation of EMT-controlling transcriptional factors Slug, Zeb1 and Zeb2. Taken together, we demonstrated that GATA3 acetylation at lysine 119 by CBP hinders the migration and invasion of lung adenocarcinoma cells. (C) 2018 Elsevier Inc. All rights reserved.