Evidence map›Paper›PMID 41274341›Full record

ArticleThe American journal of pathology2026

YAP and TEAD Are Transcriptional Regulators of Neuroendocrine Differentiation and Growth in Carcinoid Cells.

Jina Nanayakkara, Xiaojing Yang, Simona Damiani, Tashifa Imtiaz, Xiantao Wang, Dimitrios G Anastasakis, Girish M Shah, Kathrin Tyryshkin, Markus Hafner, Xiaolong Yang and 1 more

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Article in The American journal of pathology, 2026. 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

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

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.

Jina NanayakkaraLaboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Xiaojing YangLaboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Simona DamianiLaboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Tashifa ImtiazLaboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Xiantao WangRNA Molecular Biology Laboratory, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland.
Dimitrios G AnastasakisRNA Molecular Biology Laboratory, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland.
Girish M ShahCentre Hospitalier Universitaire de Québec Université Laval, Faculty of Medicine, Department of Molecular Biology, Medical Biochemistry and Pathology, Laval University, Québec, Québec, Canada.
Kathrin TyryshkinLaboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Markus HafnerRNA Molecular Biology Laboratory, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Maryland.
Xiaolong YangCancer Research Laboratory, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada.
Neil RenwickLaboratory of Translational RNA Biology, Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada. Electronic address: neil.renwick@queensu.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Molecular regulators of variably aggressive carcinoid tumors are unknown. Since carcinoids have low expression of Yes-associated protein (YAP), it was hypothesized that low YAP expression provides a molecular advantage to carcinoids by preventing YAP from binding its partner, TEA domain transcription factor (TEAD). To test this hypothesis, constitutively active YAP and a TEAD-binding defective form of YAP were overexpressed in lung (H727) and pancreatic (BON1) carcinoid cells. It was found that active YAP overexpression inhibited neuroendocrine markers, morphology, cell proliferation, and anchorage-independent cell growth, whereas TEAD-binding defective YAP recovered these features. Through integrated chromatin immunoprecipitation and RNA sequencing analyses, it was found that YAP-TEAD binding down-regulated neuroendocrine transcription factor genes and up-regulated select transforming growth factor (TGF-β) superfamily and Notch genes related to cell growth. It was concluded that low YAP expression permits neuroendocrine differentiation and growth in carcinoid cells by preventing YAP-TEAD binding and subsequent dysregulation of gene targets. These results identify unknown molecular mechanisms in carcinoid development that may apply to the broader family of neuroendocrine cancers.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoid TumorCell DifferentiationDNA-Binding ProteinsLung NeoplasmsPancreatic NeoplasmsPhosphoproteinsTranscription FactorsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansTEA Domain Transcription FactorsYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingDNA-Binding ProteinsPhosphoproteinsTEA Domain Transcription FactorsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID41274341
PMCPMC12881680

What Socratic holds

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LicenceCC BY
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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 Socratic graph.