NatD promotes lung cancer progression by preventing histone H4 serine phosphorylation to activate Slug expression
文献类型:期刊论文
作者 | Ju, Junyi5; Chen, Aiping6; Deng, Yexuan5; Liu, Ming5; Wang, Ying5; Wang, Yadong5; Nie, Min5; Wang, Chao7; Ding, Hong8![]() |
刊名 | NATURE COMMUNICATIONS
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出版日期 | 2017-10-13 |
卷号 | 8 |
ISSN号 | 2041-1723 |
DOI | 10.1038/s41467-017-00988-5 |
文献子类 | Article |
英文摘要 | N-alpha-acetyltransferase D (NatD) mediates N-a-terminal acetylation (Nt-acetylation) of histone H4 known to be involved in cell growth. Here we report that NatD promotes the migratory and invasive capabilities of lung cancer cells in vitro and in vivo. Depletion of NatD suppresses the epithelial-to-mesenchymal transition (EMT) of lung cancer cells by directly repressing the expression of transcription factor Slug, a key regulator of EMT. We found that Nt-acetylation of histone H4 antagonizes histone H4 serine 1 phosphorylation (H4S1ph), and that downregulation of Nt-acetylation of histone H4 facilitates CK2 alpha binding to histone H4 in lung cancer cells, resulting in increased H4S1ph and epigenetic reprogramming to suppress Slug transcription to inhibit EMT. Importantly, NatD is commonly upregulated in primary human lung cancer tissues where its expression level correlates with Slug expression, enhanced invasiveness, and poor clinical outcomes. These findings indicate that NatD is a crucial epigenetic modulator of cell invasion during lung cancer progression. |
WOS关键词 | N-TERMINAL ACETYLTRANSFERASES ; TO-MESENCHYMAL-TRANSITION ; COLORECTAL-CANCER ; SACCHAROMYCES-CEREVISIAE ; ALPHA-ACETYLTRANSFERASE ; PANCREATIC-CANCER ; CELL-SURVIVAL ; ACETYLATION ; METASTASIS ; KINASE |
资助项目 | National Natural Science Foundation of China[NSFC 31470750] ; National Natural Science Foundation of China[31270811] ; National Natural Science Foundation of China[81421091] ; National Natural Science Foundation of China[2014CB542300] ; National Natural Science Foundation of China[81472820] ; National Natural Science Foundation of China[2015M571736] ; National Natural Science Foundation of China[2016M590442] ; Fundamental Research Funds for the Central Universities[020814380073] ; Fundamental Research Funds for the Central Universities[020814380081] ; National Key Scientific Instrument & Equipment Development Program of China[2012YQ03026010] ; SQJ Biotechnologies Limited[00000000] |
WOS研究方向 | Science & Technology - Other Topics |
语种 | 英语 |
WOS记录号 | WOS:000412871700012 |
出版者 | NATURE PUBLISHING GROUP |
源URL | [http://119.78.100.183/handle/2S10ELR8/272451] ![]() |
专题 | 药物发现与设计中心 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
通讯作者 | Zeng, Changjiang Kathy; Wei, Jiwu; Zhao, Quan |
作者单位 | 1.La Trobe Univ, Dept Biochem, Melbourne, Vic 3086, Australia; 2.Rockefeller Univ, Lab Chromatin Biol & Epigenet, New York, NY 10065 USA; 3.SQJ Biotechnol Ltd, Palo Alto, CA 94306 USA 4.Nanjing Univ Chinese Med, State Key Lab Cultivat Base TCM Qual & Efficacy, Nanjing 210046, Jiangsu, Peoples R China; 5.Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210023, Jiangsu, Peoples R China; 6.Nanjing Univ, Med Sch, Jiangsu Key Lab Mol Med, Nanjing 210093, Jiangsu, Peoples R China; 7.Southeast Univ, Inst Life Sci, Nanjing 210096, Jiangsu, Peoples R China; 8.Chinese Acad Sci, Shanghai Inst Mat Med, Drug Discovery & Design Ctr, State Key Lab Drug Res, Shanghai 211203, Peoples R China; 9.Univ Melbourne, Walter & Eliza Hall Inst Med Res, Dept Med Biol, Melbourne, Vic 3052, Australia; |
推荐引用方式 GB/T 7714 | Ju, Junyi,Chen, Aiping,Deng, Yexuan,et al. NatD promotes lung cancer progression by preventing histone H4 serine phosphorylation to activate Slug expression[J]. NATURE COMMUNICATIONS,2017,8. |
APA | Ju, Junyi.,Chen, Aiping.,Deng, Yexuan.,Liu, Ming.,Wang, Ying.,...&Zhao, Quan.(2017).NatD promotes lung cancer progression by preventing histone H4 serine phosphorylation to activate Slug expression.NATURE COMMUNICATIONS,8. |
MLA | Ju, Junyi,et al."NatD promotes lung cancer progression by preventing histone H4 serine phosphorylation to activate Slug expression".NATURE COMMUNICATIONS 8(2017). |
入库方式: OAI收割
来源:上海药物研究所
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