Evidence map›Paper›PMID 31212916›Full record

ReviewCells2019

Regulation of TEAD Transcription Factors in Cancer Biology.

Hyunbin D Huh, Dong Hyeon Kim, Han-Sol Jeong, Hyun Woo Park

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
15.0field-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

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 261 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Comparing YAPBiomolecules · 2026
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84 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

4 authors at 2 institutions in 1 country.

Hyunbin D HuhDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea. huhhb621@yonsei.ac.kr.
Dong Hyeon KimDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea. dhk1107@yonsei.ac.kr.
Han-Sol JeongDivision of Applied Medicine, School of Korean Medicine, Pusan National University, Yangsan, Gyeongnam 50612, Korea. jhsol33@pusan.ac.kr.ORCID 0000-0001-9452-3010
Hyun Woo ParkDepartment of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea. hwp003@yonsei.ac.kr.
Yonsei University · KRPusan National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcriptional enhanced associate domain (TEAD) transcription factors play important roles during development, cell proliferation, regeneration, and tissue homeostasis. TEAD integrates with and coordinates various signal transduction pathways including Hippo, Wnt, transforming growth factor beta (TGFβ), and epidermal growth factor receptor (EGFR) pathways. TEAD deregulation affects well-established cancer genes such as KRAS, BRAF, LKB1, NF2, and MYC, and its transcriptional output plays an important role in tumor progression, metastasis, cancer metabolism, immunity, and drug resistance. To date, TEADs have been recognized to be key transcription factors of the Hippo pathway. Therefore, most studies are focused on the Hippo kinases and YAP/TAZ, whereas the Hippo-dependent and Hippo-independent regulators and regulations governing TEAD only emerged recently. Deregulation of the TEAD transcriptional output plays important roles in tumor progression and serves as a prognostic biomarker due to high correlation with clinicopathological parameters in human malignancies. In addition, discovering the molecular mechanisms of TEAD, such as post-translational modifications and nucleocytoplasmic shuttling, represents an important means of modulating TEAD transcriptional activity. Collectively, this review highlights the role of TEAD in multistep-tumorigenesis by interacting with upstream oncogenic signaling pathways and controlling downstream target genes, which provides unprecedented insight and rationale into developing TEAD-targeted anticancer therapeutics.

Indexed as

AnimalsEpithelial-Mesenchymal TransitionGenes, NeoplasmHumansNeoplasmsSignal TransductionTranscription FactorsTranscription, GeneticTranscription FactorscancerHippo pathwaystem cellTEAD

Identifiers

PMID31212916
PMCPMC6628201
OpenAlexW2952930574

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.