Evidence map›Paper›PMID 38987584›Full record

ArticleNature communications2024

The Hippo pathway transcription factors YAP and TAZ play HPV-type dependent roles in cervical cancer.

Molly R Patterson, Joseph A Cogan, Rosa Cassidy, Daisy A Theobald, Miao Wang, James A Scarth, Chinedu A Anene, Adrian Whitehouse, Ethan L Morgan, Andrew Macdonald

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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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

10 authors.

Molly R PattersonSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK. molly.patterson@pennmedicine.upenn.edu.ORCID 0000-0001-6246-7181
Joseph A CoganSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.ORCID 0009-0005-9620-7149
Rosa CassidySchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.
Daisy A TheobaldSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.
Miao WangSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.
James A ScarthBarts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0002-0076-6853
Chinedu A AneneBarts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0002-3591-3358
Adrian WhitehouseSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.ORCID 0000-0003-3866-7110
Ethan L MorganSchool of Life Sciences, University of Sussex, Brighton, UK.ORCID 0000-0002-6487-5450
Andrew MacdonaldSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK. a.macdonald@leeds.ac.uk.ORCID 0000-0002-5978-4693

Funding

Biotechnology and Biological Sciences Research Council BB/M011151/1Medical Research Council MR/S001697/1RCUK | Biotechnology and Biological Sciences Research Council (BBSRC) BB/T007222/1RCUK | Medical Research Council (MRC) MR/W006944/1RCUK | Medical Research Council (MRC) MR/X009564/1Wellcome TrustWellcome Trust 1052221/Z/14/ZWellcome Trust 204825/Z/16/Z
6 · The paper itself

Abstract

Human papillomaviruses (HPVs) cause most cervical cancers and an increasing number of anogenital and oral carcinomas, with most cases caused by HPV16 or HPV18. HPV hijacks host signalling pathways to promote carcinogenesis. Understanding these interactions could permit identification of much-needed therapeutics for HPV-driven malignancies. The Hippo signalling pathway is important in HPV+ cancers, with the downstream effector YAP playing a pro-oncogenic role. In contrast, the significance of its paralogue TAZ remains largely uncharacterised in these cancers. We demonstrate that TAZ is dysregulated in a HPV-type dependent manner by a distinct mechanism to that of YAP and controls proliferation via alternative cellular targets. Analysis of cervical cancer cell lines and patient biopsies revealed that TAZ expression was only significantly increased in HPV18+ and HPV18-like cells and TAZ knockdown reduced proliferation, migration and invasion only in HPV18+ cells. RNA-sequencing of HPV18+ cervical cells revealed that YAP and TAZ have distinct targets, suggesting they promote carcinogenesis by different mechanisms. Thus, in HPV18+ cancers, YAP and TAZ play non-redundant roles. This analysis identified TOGARAM2 as a previously uncharacterised TAZ target and demonstrates its role as a key effector of TAZ-mediated proliferation, migration and invasion in HPV18+ cancers.

Indexed as

Adaptor Proteins, Signal TransducingCell ProliferationHippo Signaling PathwayHuman papillomavirus 18Papillomavirus InfectionsProtein Serine-Threonine KinasesSignal TransductionTranscription FactorsUterine Cervical NeoplasmsYAP-Signaling ProteinsCarcinogenesisCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHuman papillomavirus 16Adaptor Proteins, Signal TransducingProtein Serine-Threonine KinasesTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID38987584
PMCPMC11237029

What OpenQuestion 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 OpenQuestion graph.