Evidence map›Paper›PMID 33419295›Full record

ArticleCancers2020

The YAP/TEAD Axis as a New Therapeutic Target in Osteosarcoma: Effect of Verteporfin and CA3 on Primary Tumor Growth.

Sarah Morice, Mathilde Mullard, Regis Brion, Maryne Dupuy, Sarah Renault, Robel Tesfaye, Bénédicte Brounais-Le Royer, Benjamin Ory, Françoise Redini, Franck Verrecchia

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

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  10. Emerging roles of long non-coding RNAs in osteosarcoma.Frontiers in molecular biosciences · 2024
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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 at 2 institutions in 1 country.

Sarah MoriceINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.
Mathilde MullardINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.
Regis BrionCHU Hôtel Dieu, F-44035 Nantes, France.
Maryne DupuyINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.
Sarah RenaultINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.
Robel TesfayeINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.ORCID 0000-0003-2358-219X
Bénédicte Brounais-Le RoyerINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.ORCID 0000-0002-4556-9853
Benjamin OryINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.ORCID 0000-0002-2622-7356
Françoise RediniINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.
Franck VerrecchiaINSERM UMR1238 "Bone Sarcomas and Remodeling of Calcified Tissues", Nantes University, F-44035 Nantes, France.ORCID 0000-0003-4920-2554
Inserm · FRHôtel-Dieu de Paris · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although some studies suggested that disruption of the Hippo signaling pathway is associated with osteosarcoma progression, the molecular mechanisms by which YAP regulates primary tumor growth is not fully clarified. In addition, the validation of YAP as a therapeutic target through the use of inhibitors in a preclinical model must be demonstrated. RNA-seq analysis and Kaplan-Meier assays identified a YAP signature in osteosarcoma patients and a correlation with patients' outcomes. Molecular and cellular analysis (RNAseq, PLA, immunoprecipitation, promoter/specific gene, proliferation, cell cycle assays) using overexpression of mutated forms of YAP able or unable to interact with TEAD, indicate that TEAD is crucial for YAP-driven cell proliferation and in vivo tumor growth. In addition, in vivo experiments using an orthotopic mice model of osteosarcoma show that two YAP/TEAD inhibitors, verteporfin and CA3, reduce primary tumor growth. In this context, in vitro experiments demonstrate that these inhibitors decrease YAP expression, YAP/TEAD transcriptional activity and cell viability mainly by their ability to induce cell apoptosis. We thus demonstrate that the YAP/TEAD signaling axis is a central actor in mediating primary tumor growth of osteosarcoma, and that the use of YAP inhibitors may be a promising therapeutic strategy against osteosarcoma tumor growth.

Indexed as

CA3Hippo/YAPosteosarcomatumor growthverteporfin

Identifiers

PMID33419295
PMCPMC7766439
OpenAlexW3115089500

What OpenQuestion holds

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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.