Evidence map›Paper›PMID 24810989›Full record

ArticleOncotarget2014

YAP1 acts as oncogenic target of 11q22 amplification in multiple cancer subtypes.

Erica Lorenzetto, Monica Brenca, Mattia Boeri, Carla Verri, Elena Piccinin, Patrizia Gasparini, Federica Facchinetti, Sabrina Rossi, Giuliana Salvatore, Maura Massimino and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

44 citing papers in PubMed, 74 citations in OpenAlex.

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  10. An overview of the crosstalk between YAP and cGAS-STING signaling in non-small cell lung cancer: it takes two to tango.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
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  17. Clinicopathologic significance of nuclear HER4 and phospho-YAP(STherapeutic advances in medical oncology · 2020
    Article
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  20. Comprehensive Genetic Characterization of Human Thyroid Cancer Cell Lines: A Validated Panel for Preclinical Studies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
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

13 authors at 7 institutions in 3 countries.

Erica LorenzettoExperimental Oncology 1, Aviano National Cancer Institute, Aviano (PN), Italy.
Monica Brenca
Mattia Boeri
Carla Verri
Elena Piccinin
Patrizia Gasparini
Federica Facchinetti
Sabrina Rossi
Giuliana Salvatore
Maura Massimino
Gabriella Sozzi
Roberta Maestro
Piergiorgio Modena
National Cancer Institute · UATumour Institute of Tuscany · ITCa' Foncello Hospital · ITEuropean Institute of Oncology · ITFederico II University Hospital · ITNational Cancer Institute · MYOspedale Sant'Anna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcriptional coactivator YAP1 is a critical effector of the human Salvador-Warts-Hippo pathway. Literature data report apparently discrepant results on the carcinogenic role of YAP1, which acts either as oncogene or as tumor suppressor in different in vitro and in vivo models. Furthermore, genomic amplification events of 11q22 locus encompassing YAP1 gene have been detected in multiple tumor types but there is limited direct evidence about the oncogenic role of endogenous YAP1 within in the amplicon. We screened a panel of human tumor samples and cancer cell lines and identified that the YAP1 amplification event is actually present in up to 23% of the cases. We exploited EKVX (lung cancer), CaSki (cervical cancer) and RO82 (thyroid cancer) cell lines harboring both genomic YAP1 amplification and YAP1 protein overexpression, in order to study the effects of downregulation of endogenous YAP1 by RNA-interference strategies. Class comparison analysis of gene expression profiling data identified 707 statistically significantly modulated genes (multivariable global test p-value = 0.002) that were functionally annotated for cell proliferation and cellular movement ontologies. Mechanistic studies of the identified perturbed pathways revealed that YAP1 silencing significantly decreased cell proliferation and cell cycle perturbation associated with upregulation of p21 and p27 cell-cycle inhibitors, reduced cell migration (p<0.048) and anchorage-independent growth (p<0.02). In CaSki cell line, YAP1 silencing induced significantly increased sensitivity and cell-death response to cisplatin treatment (p=0.011) as well as reduction of in-vivo tumorigenic potential (p=0.027). Overall, these results establish that YAP1 is a direct oncogenic target of the 11q22 amplicon in previously unreported cancer types and support the relevance of such genetic aberration in carcinogenesis in a fraction of multiple tumor types.

Indexed as

Gene AmplificationAdaptor Proteins, Signal TransducingAntineoplastic AgentsApoptosisCell CycleCell MovementCell ProliferationCell Transformation, NeoplasticChemotaxisChromosomes, Human, Pair 11CisplatinFemaleHumansIn Situ Hybridization, FluorescenceLung NeoplasmsPhosphoproteinsAdaptor Proteins, Signal TransducingAntineoplastic AgentsCisplatinPhosphoproteinsRNA, MessengerTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID24810989
PMCPMC4058031
OpenAlexW2152093423

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.