Evidence map›Paper›PMID 36806855›Full record

ArticleJournal of molecular cell biology2023

Tea domain transcription factor TEAD4 mitigates TGF-β signaling and hepatocellular carcinoma progression independently of YAP.

Weicheng Luo, Yi Li, Yi Zeng, Yining Li, Minzhang Cheng, Cheng Zhang, Fei Li, Yiqing Wu, Chunhong Huang, Xiaolong Yang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 10 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

18 authors at 6 institutions in 4 countries.

Weicheng LuoDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Yi LiDepartment of Rheumatology and Clinical Immunology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang 330006, China.
Yi ZengDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Yining LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Minzhang ChengCenter for Experimental Medicine, The First Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Cheng ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Fei LiDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Yiqing WuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Chunhong HuangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Xiaolong YangDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, ON K7L 3N6, Canada.
Joachim KremerskothenDepartment of Nephrology, Hypertension and Rheumatology, University Hospital Münster, Münster 48149, Germany.
Jianmin ZhangDepartment of Cancer Genetics & Genomics, Roswell Park Comprehensive Cancer Center, Elm and Carlton Streets, Buffalo, NY 14203, USA.
Chunbo ZhangSchool of Pharmacy, Nanchang University Jiangxi Medical College, Nanchang 330008, China.
Shuo TuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.
Zhihua LiKey Laboratory of Breast Diseases of Jiangxi Province, Nanchang People's Hospital, Nanchang 330025, China.
Zhijun LuoDepartment of Pathology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330006, China.ORCID 0000-0001-8105-5289
Zhenghong LinSchool of Life Sciences, Chongqing University, Chongqing 405200, China.
Xiaohua YanDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Nanchang University Jiangxi Medical College, Nanchang 330031, China.ORCID 0000-0002-7528-5771
Nanchang University · CNChongqing University · CNJiangxi Provincial People's Hospital · CNQueen's University · CARoswell Park Comprehensive Cancer Center · USUniversity Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tea domain transcription factor 4 (TEAD4) plays a pivotal role in tissue development and homeostasis by interacting with Yes-associated protein (YAP) in response to Hippo signaling inactivation. TEAD4 and YAP can also cooperate with transforming growth factor-β (TGF-β)-activated Smad proteins to regulate gene transcription. Yet, it remains unclear whether TEAD4 plays a YAP-independent role in TGF-β signaling. Here, we unveil a novel tumor suppressive function of TEAD4 in liver cancer via mitigating TGF-β signaling. Ectopic TEAD4 inhibited TGF-β-induced signal transduction, Smad transcriptional activity, and target gene transcription, consequently suppressing hepatocellular carcinoma cell proliferation and migration in vitro and xenograft tumor growth in mice. Consistently, depletion of endogenous TEAD4 by siRNAs enhanced TGF-β signaling in cancer cells. Mechanistically, TEAD4 associates with receptor-regulated Smads (Smad2/3) and Smad4 in the nucleus, thereby impairing the binding of Smad2/3 to the histone acetyltransferase p300. Intriguingly, these negative effects of TEAD4 on TGF-β/Smad signaling are independent of YAP, as impairing the TEAD4-YAP interaction through point mutagenesis or depletion of YAP and/or its paralog TAZ has little effect. Together, these results unravel a novel function of TEAD4 in fine tuning TGF-β signaling and liver cancer progression in a YAP-independent manner.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsTEA Domain Transcription FactorsAdaptor Proteins, Signal TransducingAnimalsHumansMiceSignal TransductionTransforming Growth Factor betaYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingTEAD4 protein, humanTEA Domain Transcription FactorsTransforming Growth Factor betaYAP-Signaling Proteinshepatocellular carcinomap300signaling regulationTEAD4TGF-βtranscriptional activity

Identifiers

PMID36806855
PMCPMC10446140
OpenAlexW4321478370

What OpenQuestion holds

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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.