globalchange  > 全球变化的国际研究计划
DOI: 10.1002/1873-3468.13549
WOS记录号: WOS:000481196300001
论文题名:
Global changes in chromatin accessibility and transcription following ATRX inactivation in human cancer cells
作者: Liang, Junbo1; Liu, Hongchao1; Li, Guangyu1; Qian, Jun1; Gao, Ran1; Zhou, Yanchi2; Wang, Xiaoyue1
通讯作者: Wang, Xiaoyue
刊名: FEBS LETTERS
ISSN: 0014-5793
EISSN: 1873-3468
出版年: 2019
语种: 英语
英文关键词: ATAC-seq ; ATRX ; heterochromatin ; TGF-beta
WOS关键词: READ ALIGNMENT ; COHESIN ; H3.3 ; SEQ ; DAXX/ATRX ; ELEMENTS ; PROTEIN ; GENES
WOS学科分类: Biochemistry & Molecular Biology ; Biophysics ; Cell Biology
WOS研究方向: Biochemistry & Molecular Biology ; Biophysics ; Cell Biology
英文摘要:

alpha-Tthalassemia mental retardation X-linked (ATRX) is a chromatin remodeler frequently mutated in many cancers. Despite the binding pattern of ATRX in heterochromatin, ATRX-mediated epigenomic changes in cancer cells have not been profiled, especially for the heterochromatin regions. Here, we profiled genome-wide maps of chromatin accessibility in ATRX-intact and ATRX-null human cancer cells. We found extensive changes in chromatin accessibility in both repetitive DNA regions and non-repetitive regulatory regions following ATRX loss. These changes are highly correlated with changes in transcription, which lead to alterations in cancer-related signalling pathways, such as upregulation of the TGF-beta pathway and downregulation of the cadherin family of proteins. These findings indicate that ATRX deficiency induces epigenomic changes and promotes tumorigenesis through both genome instability and shifts in transcription.


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资源类型: 期刊论文
标识符: http://119.78.100.158/handle/2HF3EXSE/145280
Appears in Collections:全球变化的国际研究计划

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作者单位: 1.Chinese Acad Med Sci, Peking Union Med Coll, Inst Basic Med Sci, State Key Lab Med Mol Biol, Beijing 100005, Peoples R China
2.Chinese Acad Med Sci, Canc Hosp, Peking Union Med Coll, Natl Canc Ctr, Beijing, Peoples R China

Recommended Citation:
Liang, Junbo,Liu, Hongchao,Li, Guangyu,et al. Global changes in chromatin accessibility and transcription following ATRX inactivation in human cancer cells[J]. FEBS LETTERS,2019-01-01
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