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

Wenyi Mi, Haipeng Guan, Jie Lyu, Dan Zhao, Yuanxin Xi, Shiming Jiang, Forest H. Andrews, Xiaolu Wang, Mihai Gagea, Hong Wen, Laszlo Tora, Sharon Y. R. Dent, Tatiana G. Kutateladze, Wei Li (), Haitao Li () and Xiaobing Shi ()
Additional contact information
Wenyi Mi: The University of Texas M.D. Anderson Cancer Center
Haipeng Guan: MOE Key Laboratory of Protein Sciences, Beijing Advanced Innovation Center for Structural Biology, Department of Basic Medical Sciences, School of Medicine, Tsinghua University
Jie Lyu: Dan L. Duncan Cancer Center, Baylor College of Medicine
Dan Zhao: MOE Key Laboratory of Protein Sciences, Beijing Advanced Innovation Center for Structural Biology, Department of Basic Medical Sciences, School of Medicine, Tsinghua University
Yuanxin Xi: Dan L. Duncan Cancer Center, Baylor College of Medicine
Shiming Jiang: The University of Texas M.D. Anderson Cancer Center
Forest H. Andrews: University of Colorado School of Medicine
Xiaolu Wang: The University of Texas M.D. Anderson Cancer Center
Mihai Gagea: The University of Texas M.D. Anderson Cancer Center
Hong Wen: The University of Texas M.D. Anderson Cancer Center
Laszlo Tora: Institut de Génétique et de Biologie Moléculaire et Cellulaire
Sharon Y. R. Dent: The University of Texas M.D. Anderson Cancer Center
Tatiana G. Kutateladze: University of Colorado School of Medicine
Wei Li: Dan L. Duncan Cancer Center, Baylor College of Medicine
Haitao Li: MOE Key Laboratory of Protein Sciences, Beijing Advanced Innovation Center for Structural Biology, Department of Basic Medical Sciences, School of Medicine, Tsinghua University
Xiaobing Shi: The University of Texas M.D. Anderson Cancer Center

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract 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.

Date: 2017
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-017-01173-4 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01173-4

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-017-01173-4

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().