Evidence map›Paper›PMID 35835915›Full record

ArticleNature genetics2022

YAP induces an oncogenic transcriptional program through TET1-mediated epigenetic remodeling in liver growth and tumorigenesis.

Bo-Kuan Wu, Szu-Chieh Mei, Elizabeth H Chen, Yonggang Zheng, Duojia Pan

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
9.0field-weighted citation impact, top 1% of its field
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

55 citing papers in PubMed, 83 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Bo-Kuan WuDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Szu-Chieh MeiDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Elizabeth H ChenDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Yonggang ZhengDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-3326-4614
Duojia PanDepartment of Physiology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. duojia.pan@utsouthwestern.edu.ORCID http://orcid.org/0000-0003-2890-4645
Howard Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Control of Cell Number in Developing RetinaR01EY015708 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI DUOJIA PAN · 2004 to 2026
$8.8M
UT Southwestern NORCP30DK127984 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JAY D. HORTON · 2022 to 2026
$7.4M
Molecular Mechanisms of Myoblast FusionR01AR053173 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI CHEN, ELIZABETH H · 2006 to 2022
$5.3M
Decoding the mechanisms of cell-cell fusion - Renewal - 1R35GM136316 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Elizabeth H Chen · 2020 to 2026
$3.1M
Howard Hughes Medical InstituteNEI NIH HHS R01 EY015708NIAMS NIH HHS R01 AR053173NIDDK NIH HHS P30 DK127984NIGMS NIH HHS R35 GM136316
6 · The paper itself

Abstract

Epigenetic remodeling is essential for oncogene-induced cellular transformation and malignancy. In contrast to histone post-translational modifications, how DNA methylation is remodeled by oncogenic signaling remains poorly understood. The oncoprotein YAP, a coactivator of the TEAD transcription factors mediating Hippo signaling, is widely activated in human cancers. Here, we identify the 5-methylcytosine dioxygenase TET1 as a direct YAP target and a master regulator that coordinates the genome-wide epigenetic and transcriptional reprogramming of YAP target genes in the liver. YAP activation induces the expression of TET1, which physically interacts with TEAD to cause regional DNA demethylation, histone H3K27 acetylation and chromatin opening in YAP target genes to facilitate transcriptional activation. Loss of TET1 not only reverses YAP-induced epigenetic and transcriptional changes but also suppresses YAP-induced hepatomegaly and tumorigenesis. These findings exemplify how oncogenic signaling regulates the site specificity of DNA demethylation to promote tumorigenesis and implicate TET1 as a potential target for modulating YAP signaling in physiology and disease.

Indexed as

DNA-Binding ProteinsTranscription FactorsCarcinogenesisCell Cycle ProteinsEpigenesis, GeneticHistonesHumansLiverMixed Function OxygenasesOncogenesProto-Oncogene ProteinsCell Cycle ProteinsDNA-Binding ProteinsHistonesMixed Function OxygenasesProto-Oncogene ProteinsTET1 protein, humanTranscription FactorsYY1AP1 protein, human

Identifiers

PMID35835915
PMCPMC9357225
OpenAlexW4285388619

What OpenQuestion holds

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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.