Evidence map›Paper›PMID 41214656›Full record

ArticleBMC oral health2025

Design and biological evaluation of peptide disruptors targeting YAP1-TEAD interaction for oral cancer.

Yue Wu, Hao Yang, Xianglei Zhang, Lu Liu, Yu Liu, Chao Xu, Kailiu Wu, Guanying Feng, Weijia Xu, Xi Yang and 1 more

Abstract read
In one paragraph

Article in BMC oral health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Yue Wu *Department of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China.ORCID 0000-0002-5413-0420
Hao Yang *Shanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.ORCID 0009-0008-0040-276X
Xianglei ZhangShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Lu LiuShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Yu LiuDepartment of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China.
Chao XuShanghai Institute for Advanced Immunochemical Studies and School of Life Science and Technology, ShanghaiTech University, Shanghai, 201210, China.
Kailiu WuDepartment of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China.
Guanying FengDepartment of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China.
Weijia XuDepartment of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China.
Xi YangDepartment of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China. yangxi16@163.com.
Chenping ZhangDepartment of Oral Maxillofacial-Head Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology, Shanghai, 200011, China. Zhang.chenping@hotmail.com.ORCID 0009-0002-4399-5792

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have highlighted the critical role of the Yes associated protein 1 - TEA domain transcription factor (YAP1-TEAD) interaction in the progression of oral cancer. However, there remains a lack of direct disruptors targeting the YAP1-TEAD protein interaction and a detailed investigation of their effects on oral cancer. Therefore, we aimed to rationally design peptide YAP1-TEAD protein interaction disruptors through computational methods and explore the effects of direct disruption of the YAP1-TEAD interaction in oral squamous cell carcinoma (OSCC).

methodsPeptide-based computational residue scanning was employed to design peptide disruptors of YAP1-TEAD interaction by analyzing the effects of mutations on binding affinity and stability. Molecular dynamics (MD) simulations were performed to assess the binding affinity and stability from a dynamic perspective. Surface plasmon resonance (SPR) assays were used to assess the in vitro binding affinities. After three rounds of iterative optimization, two with the highest affinities of this series of disruptors were applied to OSCC cell lines to investigate the primary effects of direct disruption of the YAP1-TEAD interaction.

resultsThe expression of YAP1, TEADs, and four downstream transcriptional targets were significantly higher in OSCC tissues compared to paired normal tissues. The design and evaluation of YAP1-TEAD disruptors were conducted using computational residue scanning, MD simulations, and SPR assays. After three rounds of optimization, YTPD9 and YTPD11 demonstrated the highest affinities, with binding affinities 10 times more than that of the wildtype YAP1. When applied to OSCC cell lines, the disruptors exhibited a limited effect on cell proliferation, but they were able to inhibit the abilities of migration and invasion effectively.

conclusionThis study developed a series of peptide disruptors targeting YAP1-TEAD protein interaction through computational simulations and in vitro experiments. The biological evaluation of two of these disruptors in OSCC confirmed that direct disruption of the YAP1-TEAD primarily affects the migration and invasion ability of oral cancer.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoma, Squamous CellDNA-Binding ProteinsMouth NeoplasmsPeptidesTranscription FactorsCell Line, TumorCell ProliferationHumansMolecular Dynamics SimulationProtein BindingSurface Plasmon ResonanceTEA Domain Transcription FactorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingDNA-Binding ProteinsPeptidesTEA Domain Transcription FactorsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsMolecular dynamics simulationOral cancerPPI disruptorYAP1-TEAD interaction

Identifiers

PMID41214656
PMCPMC12599100

What Socratic holds

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Registered trials

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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 Socratic graph.