Evidence map›Paper›PMID 25974963›Full record

ArticleOncotarget2015

YM155 potently triggers cell death in breast cancer cells through an autophagy-NF-kB network.

Eloïse Véquaud, Céline Séveno, Delphine Loussouarn, Lucie Engelhart, Mario Campone, Philippe Juin, Sophie Barillé-Nion

Abstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Review
  9. Small Molecules Targeting Programmed Cell Death in Breast Cancer Cells.International journal of molecular sciences · 2021
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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

7 authors.

Eloïse VéquaudCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.
Céline SévenoCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.
Delphine LoussouarnCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.
Lucie EngelhartCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.
Mario CamponeCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.
Philippe JuinCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.
Sophie Barillé-NionCRCNA, UMR INSERM U892, CNRS 6299, Université de Nantes, Team 8 « Cell Survival and Tumor Escape in Breast Cancers », Institut de Recherche en Santé de l'Université de Nantes, Nantes, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Specific overexpression in cancer cells and evidence of oncogenic functions make Survivin an attractive target in cancer therapy. The small molecule compound YM155 has been described as the first "Survivin suppressant" but molecular mechanisms involved in its biological activity and its clinical potential remain obscure. We herein show that YM155 exerts single agent toxicity on primary breast cancer cells grown in an ex vivo assay preserving tumor microenvironment. In vitro assays indicate that YM155 more efficiently triggers cell death in breast cancer cells (including these with stem-cell like properties) than in non tumorigenic mammary cells. YM155-induced cell death is critically dependent on autophagy and NF-kB but independent of p53 and it coïncides with DNA damage and a DNA damage response in p53-proficient cells. Our results point out a crosstalk between NF-kB and autophagy controlling YM155-induced death in breast cancer cells and argue for the potential use of YM155 as a genotoxic agent in breast cancer therapy.

Indexed as

Antineoplastic AgentsAutophagyBreast NeoplasmsCell DeathCell Line, TumorCell ProliferationDNA DamageFemaleHumansImidazolesMCF-7 CellsNaphthoquinonesNF-kappa BSignal TransductionTransfectionXenograft Model Antitumor AssaysAntineoplastic AgentsImidazolesNaphthoquinonesNF-kappa Bsepantroniumbreast cancerex vivo assaytherapy

Identifiers

PMID25974963
PMCPMC4537028

What OpenQuestion holds

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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.