Evidence map›Paper›PMID 42217442›Full record

ArticleNeoplasia (New York, N.Y.)2026

Systematic analysis of hippo pathway signaling identifies TEAD1 as a transcriptional regulator of neuroendocrine prostate cancer.

Lisha G Brown, Ilsa M Coleman, Tony L H Chu, Erolcan Sayar, Radhika A Patel, Brian Hanratty, Mohamed Adil, Dapei Li, Yongtao Li, Holly M Nguyen and 14 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

24 authors.

Lisha G BrownDepartment of Urology, University of Washington, Seattle, WA, USA.
Ilsa M ColemanDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Tony L H ChuDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Erolcan SayarDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Radhika A PatelDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Brian HanrattyDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Mohamed AdilDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA; Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Dapei LiDepartment of Medicine, Division of Medical Oncology, University of Washington, Seattle, WA, USA.
Yongtao LiDepartment of Urology, University of Washington, Seattle, WA, USA.
Holly M NguyenDepartment of Urology, University of Washington, Seattle, WA, USA.
Conner J SessionsDepartment of Urology, University of Washington, Seattle, WA, USA.
Erin L SweeneyDepartment of Urology, University of Washington, Seattle, WA, USA.
Joshi J AlumkalDepartment of Internal Medicine, Rogel Cancer Center, University of Michigan, Ann Arbor, MI, USA.
Rui M Gil da CostaDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Yuzhuo WangDepartment of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada.
Daniel W LinDepartment of Urology, University of Washington, Seattle, WA, USA.
Lawrence D TrueDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Ruth DumpitDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA.
Eva CoreyDepartment of Urology, University of Washington, Seattle, WA, USA.
John K LeeDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA; Division of Hematology/Oncology, Department of Medicine University of California Los Angeles Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA.
Peter S NelsonDepartment of Urology, University of Washington, Seattle, WA, USA; Division of Clinical Research, Fred Hutchinson Cancer Center, Seattle, WA, USA; Department of Medicine, Division of Medical Oncology, University of Washington, Seattle, WA, USA.
Li XinDepartment of Urology, University of Washington, Seattle, WA, USA.
Michael C HaffnerDivision of Human Biology, Fred Hutchinson Cancer Center, Seattle, WA, USA; Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA; Division of Clinical Research, Fred Hutchinson Cancer Center, Seattle, WA, USA. Electronic address: mhaffner@fredhutch.org.
Colm MorrisseyDepartment of Urology, University of Washington, Seattle, WA, USA. Electronic address: cmorriss@uw.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment-induced neuroendocrine prostate cancer (NEPC) represents an aggressive form of castration-resistant prostate cancer (CRPC) associated with lineage plasticity and therapeutic resistance. In this study, we investigated the role of the Hippo signaling axis in the transdifferentiation from androgen receptor-positive prostate cancer (ARPC) to NEPC. RNA sequencing analyses of CRPC metastases revealed coordinated alterations in Hippo pathway components, with decreased expression of YAP1, LATS2, and TEAD2 and increased expression of LATS1, TEAD1, and the RNA splicing regulator RBFOX2 in NEPC. These transcriptional alterations were consistently observed across multiple model systems and patient samples. Epigenetic analyses demonstrated that reduced expression of YAP1, TEAD2, and LATS2 was associated with increased DNA methylation, whereas elevated TEAD1 expression correlated with DNA hypomethylation in NEPC. NEPC selectively retained TEAD1 expression, including a spliced isoform not detected in ARPC. Proteomic interactome analyses revealed that TEAD1 associated with RNA splicing factors and DNA repair proteins. Functional studies showed that TEAD1 knockdown led to the reversion of gene programs associated with epithelial differentiation. These findings indicate that the conversion of ARPC to NEPC involves coordinated loss of AR, YAP1, and REST activity alongside sustained TEAD1 expression and altered RNA processing. Our data identify TEAD1 as a transcriptional regulator associated with the NEPC state and suggest a role for TEAD1-linked transcriptional and post-transcriptional mechanisms in prostate cancer lineage plasticity.

Indexed as

Carcinoma, NeuroendocrineDNA-Binding ProteinsGene Expression Regulation, NeoplasticNeuroendocrine TumorsNuclear ProteinsProstatic NeoplasmsProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsAnimalsCell Line, TumorDNA MethylationHippo Signaling PathwayHumansMaleTEA Domain Transcription FactorsDNA-Binding ProteinsNuclear ProteinsProtein Serine-Threonine KinasesTEAD1 protein, humanTEA Domain Transcription FactorsTranscription FactorsNeuroendocrineProstateRBFOX2TEAD1YAP

Identifiers

PMID42217442
PMCPMC13241777

What Socratic 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 Socratic graph.