Evidence map›Paper›PMID 25848952›Full record

ArticlePloS one2015

Transcriptome analysis of Wnt3a-treated triple-negative breast cancer cells.

Sylvie Maubant, Bruno Tesson, Virginie Maire, Mengliang Ye, Guillem Rigaill, David Gentien, Francisco Cruzalegui, Gordon C Tucker, Sergio Roman-Roman, Thierry Dubois

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.0field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

  1. Pooled it
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  15. International journal of molecular sciences · 2023
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  19. Translocon-associated Protein Subunit SSR3 Determines and Predicts Susceptibility to Paclitaxel in Breast Cancer and Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
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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 4 institutions in 1 country.

Sylvie MaubantBreast Cancer Biology Group, Translational Research Department, Institut Curie, Centre de Recherche, Paris, France.
Bruno TessonBreast Cancer Biology Group, Translational Research Department, Institut Curie, Centre de Recherche, Paris, France; INSERM U900, Bioinformatics, Biostatistics, Epidemiology and Computational Systems Biology of Cancer, Institut Curie, Centre de Recherche, Paris, France; Mines ParisTech, Fontainebleau, France.
Virginie MaireBreast Cancer Biology Group, Translational Research Department, Institut Curie, Centre de Recherche, Paris, France.
Mengliang YeBreast Cancer Biology Group, Translational Research Department, Institut Curie, Centre de Recherche, Paris, France.
Guillem RigaillUnité de Recherche en Génomique Végétale, INRA-CNRS-Université d'Evry Val d'Essonne, Evry, France.
David GentienPlatform of Molecular Biology Facilities, Translational Research Department, Institut Curie, Centre de Recherche, Paris, France.
Francisco CruzaleguiInstitut de Recherches SERVIER, Pôle Innovation Thérapeutique Oncologie, Croissy-sur-Seine, France.
Gordon C TuckerInstitut de Recherches SERVIER, Pôle Innovation Thérapeutique Oncologie, Croissy-sur-Seine, France.
Sergio Roman-RomanTranslational Research Department, Institut Curie, Centre de Recherche, Paris, France.
Thierry DuboisBreast Cancer Biology Group, Translational Research Department, Institut Curie, Centre de Recherche, Paris, France.
Institut Curie · FRServier (France) · FRGénomique Bioinformatique et Applications · FRInstitut des Sciences des Plantes de Paris Saclay · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The canonical Wnt/β-catenin pathway is activated in triple-negative breast cancer (TNBC). The activation of this pathway leads to the expression of specific target genes depending on the cell/tissue context. Here, we analyzed the transcriptome of two different TNBC cell lines to define a comprehensive list of Wnt target genes. The treatment of cells with Wnt3a for 6h up-regulated the expression (fold change > 1.3) of 59 genes in MDA-MB-468 cells and 241 genes in HCC38 cells. Thirty genes were common to both cell lines. Beta-catenin may also be a transcriptional repressor and we found that 18 and 166 genes were down-regulated in response to Wnt3a treatment for 6h in MDA-MB-468 and HCC38 cells, respectively, of which six were common to both cell lines. Only half of the activated and the repressed transcripts have been previously described as Wnt target genes. Therefore, our study reveals 137 novel genes that may be positively regulated by Wnt3a and 104 novel genes that may be negatively regulated by Wnt3a. These genes are involved in the Wnt pathway itself, and also in TGFβ, p53 and Hedgehog pathways. Thorough characterization of these novel potential Wnt target genes may reveal new regulators of the canonical Wnt pathway. The comparison of our list of Wnt target genes with those published in other cellular contexts confirms the notion that Wnt target genes are tissue-, cell line- and treatment-specific. Genes up-regulated in Wnt3a-stimulated cell lines were more strongly expressed in TNBC than in luminal A breast cancer samples. These genes were also overexpressed, but to a much lesser extent, in HER2+ and luminal B tumors. We identified 72 Wnt target genes higher expressed in TNBCs (17 with a fold change >1.3) which may reflect the chronic activation of the canonical Wnt pathway that occurs in TNBC tumors.

Indexed as

Gene Expression ProfilingCell Line, TumorHumansTranscriptional ActivationTriple Negative Breast NeoplasmsWnt3A ProteinWnt Signaling PathwayWnt3A Protein

Identifiers

PMID25848952
PMCPMC4388387
OpenAlexW1995608074

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.