Evidence map›Paper›PMID 27340176›Full record

ArticleGenes & development2016

INO80 governs superenhancer-mediated oncogenic transcription and tumor growth in melanoma.

Bingying Zhou, Li Wang, Shu Zhang, Brian D Bennett, Fan He, Yan Zhang, Chengliang Xiong, Leng Han, Lixia Diao, Pishun Li and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

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  18. Chromatin remodellers as therapeutic targets.Nature reviews. Drug discovery · 2024
    Review
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 8 institutions in 3 countries.

Bingying ZhouState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; Department of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA;
Li WangState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China; Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Shu ZhangDepartment of Pulmonary and Critical Care Medicine, Chinese PLA General Hospital, Beijing 100853, China;
Brian D BennettIntegrative Bioinformatics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Fan HeDepartment of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China;
Yan ZhangFamily Planning Research Institute, Center of Reproductive Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China;
Chengliang XiongFamily Planning Research Institute, Center of Reproductive Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China;
Leng HanDepartment of Biochemistry and Molecular Biology, The University of Texas Health Science Center at Houston McGovern Medical School, Houston, Texas 77030, USA;
Lixia DiaoDepartment of Bioinformatics and Computational Biology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
Pishun LiEpigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
David C FargoIntegrative Bioinformatics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
Adrienne D CoxDepartment of Pharmacology, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA; Department of Radiation Oncology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, USA.
Guang HuEpigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA;
National Institute of Environmental Health Sciences · USHuazhong University of Science and Technology · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNChinese PLA General Hospital · CNFu Wai Hospital · CNInstitute of Pharmacology · CZThe University of Texas Health Science Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

Role of Pluripotency Factors in Pluripotent Stem Cells, Development and DiseaseZIAES102745 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI HU, GUANG · 2010 to 2025
$31.5M
BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
Genetic dissection and inhibitor targeting of Rac signaling in pancreatic cancer.R21CA161494 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2011 to 2012
$354k
NCI NIH HHS R01 CA042978NCI NIH HHS R21 CA161494
6 · The paper itself

Abstract

Superenhancers (SEs) are large genomic regions with a high density of enhancer marks. In cancer, SEs are found near oncogenes and dictate cancer gene expression. However, how oncogenic SEs are regulated remains poorly understood. Here, we show that INO80, a chromatin remodeling complex, is required for SE-mediated oncogenic transcription and tumor growth in melanoma. The expression of Ino80, the SWI/SNF ATPase, is elevated in melanoma cells and patient melanomas compared with normal melanocytes and benign nevi. Furthermore, Ino80 silencing selectively inhibits melanoma cell proliferation, anchorage-independent growth, tumorigenesis, and tumor maintenance in mouse xenografts. Mechanistically, Ino80 occupies >90% of SEs, and its occupancy is dependent on transcription factors such as MITF and Sox9. Ino80 binding reduces nucleosome occupancy and facilitates Mediator recruitment, thus promoting oncogenic transcription. Consistently, genes co-occupied by Ino80 and Med1 are selectively expressed in melanomas compared with melanocytes. Together, our results reveal an essential role of INO80-dependent chromatin remodeling in SE function and suggest a novel strategy for disrupting SEs in cancer treatment.

Indexed as

AnimalsCarcinogenesisCell Cycle ProteinsCell ProliferationChromatin Assembly and DisassemblyEnhancer Elements, GeneticGene Expression Regulation, NeoplasticGene SilencingHeterograftsHumansMediator Complex Subunit 1MelanocytesMelanomaMiceNuclear ProteinsProtein BindingCell Cycle ProteinsINO80B protein, humanMED1 protein, humanMediator Complex Subunit 1Nuclear ProteinsTranscription Factorschromatin remodelerINO80oncogenic transcriptionsuperenhancer

Identifiers

PMID27340176
PMCPMC4926866
OpenAlexW2465915772

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.