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YEATS2 links histone acetylation to tumorigenesis of non-small cell lung cancer

Recognition of modified histones by “reader” proteins constitutes a key mechanism regulating diverse chromatin-associated processes important for normal and neoplastic development. We recently identified the YEATS domain as a novel acetyllysine-binding module; however, the functional importance of Y... Full description

Journal Title: Nat Commun 2017, Vol.8(1), pp.1088-1088
Main Author: Mi, Wenyi
Other Authors: Guan, Haipeng , Lyu, Jie , Zhao, Dan , Xi, Yuanxin , Jiang, Shiming , Andrews, Forest , Wang, Xiaolu , Gagea, Mihai , Wen, Hong , Tora, Laszlo , Dent, Sharon , Kutateladze, Tatiana , Li, Wei , Li, Haitao , Shi, Xiaobing
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 2041-1723 ; DOI: 10.1038/s41467-017-01173-4
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recordid: palgrave_j10.1038/s41467-017-01173-4
title: YEATS2 links histone acetylation to tumorigenesis of non-small cell lung cancer
format: Article
creator:
  • Mi, Wenyi
  • Guan, Haipeng
  • Lyu, Jie
  • Zhao, Dan
  • Xi, Yuanxin
  • Jiang, Shiming
  • Andrews, Forest
  • Wang, Xiaolu
  • Gagea, Mihai
  • Wen, Hong
  • Tora, Laszlo
  • Dent, Sharon
  • Kutateladze, Tatiana
  • Li, Wei
  • Li, Haitao
  • Shi, Xiaobing
subjects:
  • Biology
ispartof: Nat Commun, 2017, Vol.8(1), pp.1088-1088
description: Recognition of modified histones by “reader” proteins constitutes a key mechanism regulating diverse chromatin-associated processes important for normal and neoplastic development. We recently identified the YEATS domain as a novel acetyllysine-binding module; however, the functional importance of YEATS domain-containing proteins in human cancer remains largely unknown. Here, we show that the YEATS2 gene is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cancer cell growth and survival. YEATS2 binds to acetylated histone H3 via its YEATS domain. The YEATS2-containing ATAC complex co-localizes with H3K27 acetylation (H3K27ac) on the promoters of actively transcribed genes. Depletion of YEATS2 or disruption of the interaction between its YEATS domain and acetylated histones reduces the ATAC complex-dependent promoter H3K9ac levels and deactivates the expression of essential genes. Taken together, our study identifies YEATS2 as a histone H3K27ac reader that regulates a transcriptional program essential for NSCLC tumorigenesis.
language: eng
source:
identifier: ISSN: 2041-1723 ; DOI: 10.1038/s41467-017-01173-4
fulltext: fulltext
issn:
  • 2041-1723
  • 20411723
url: Link


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titleYEATS2 links histone acetylation to tumorigenesis of non-small cell lung cancer
creatorMi, Wenyi ; Guan, Haipeng ; Lyu, Jie ; Zhao, Dan ; Xi, Yuanxin ; Jiang, Shiming ; Andrews, Forest ; Wang, Xiaolu ; Gagea, Mihai ; Wen, Hong ; Tora, Laszlo ; Dent, Sharon ; Kutateladze, Tatiana ; Li, Wei ; Li, Haitao ; Shi, Xiaobing
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identifierISSN: 2041-1723 ; DOI: 10.1038/s41467-017-01173-4
descriptionRecognition of modified histones by “reader” proteins constitutes a key mechanism regulating diverse chromatin-associated processes important for normal and neoplastic development. We recently identified the YEATS domain as a novel acetyllysine-binding module; however, the functional importance of YEATS domain-containing proteins in human cancer remains largely unknown. Here, we show that the YEATS2 gene is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cancer cell growth and survival. YEATS2 binds to acetylated histone H3 via its YEATS domain. The YEATS2-containing ATAC complex co-localizes with H3K27 acetylation (H3K27ac) on the promoters of actively transcribed genes. Depletion of YEATS2 or disruption of the interaction between its YEATS domain and acetylated histones reduces the ATAC complex-dependent promoter H3K9ac levels and deactivates the expression of essential genes. Taken together, our study identifies YEATS2 as a histone H3K27ac reader that regulates a transcriptional program essential for NSCLC tumorigenesis.
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titleYEATS2 links histone acetylation to tumorigenesis of non-small cell lung cancer
descriptionRecognition of modified histones by “reader” proteins constitutes a key mechanism regulating diverse chromatin-associated processes important for normal and neoplastic development. We recently identified the YEATS domain as a novel acetyllysine-binding module; however, the functional importance of YEATS domain-containing proteins in human cancer remains largely unknown. Here, we show that the YEATS2 gene is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cancer cell growth and survival. YEATS2 binds to acetylated histone H3 via its YEATS domain. The YEATS2-containing ATAC complex co-localizes with H3K27 acetylation (H3K27ac) on the promoters of actively transcribed genes. Depletion of YEATS2 or disruption of the interaction between its YEATS domain and acetylated histones reduces the ATAC complex-dependent promoter H3K9ac levels and deactivates the expression of essential genes. Taken together, our study identifies YEATS2 as a histone H3K27ac reader that regulates a transcriptional program essential for NSCLC tumorigenesis.
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authorMi, Wenyi ; Guan, Haipeng ; Lyu, Jie ; Zhao, Dan ; Xi, Yuanxin ; Jiang, Shiming ; Andrews, Forest ; Wang, Xiaolu ; Gagea, Mihai ; Wen, Hong ; Tora, Laszlo ; Dent, Sharon ; Kutateladze, Tatiana ; Li, Wei ; Li, Haitao ; Shi, Xiaobing
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abstractRecognition of modified histones by “reader” proteins constitutes a key mechanism regulating diverse chromatin-associated processes important for normal and neoplastic development. We recently identified the YEATS domain as a novel acetyllysine-binding module; however, the functional importance of YEATS domain-containing proteins in human cancer remains largely unknown. Here, we show that the YEATS2 gene is highly amplified in human non-small cell lung cancer (NSCLC) and is required for cancer cell growth and survival. YEATS2 binds to acetylated histone H3 via its YEATS domain. The YEATS2-containing ATAC complex co-localizes with H3K27 acetylation (H3K27ac) on the promoters of actively transcribed genes. Depletion of YEATS2 or disruption of the interaction between its YEATS domain and acetylated histones reduces the ATAC complex-dependent promoter H3K9ac levels and deactivates the expression of essential genes. Taken together, our study identifies YEATS2 as a histone H3K27ac reader that regulates a transcriptional program essential for NSCLC tumorigenesis.
pubNature Publishing Group UK
doi10.1038/s41467-017-01173-4
orcidid0000-0002-7453-051X
pages1088
date2017-12