Evidence map›Paper›PMID 26497683›Full record

ArticleOncotarget2015

A novel prohibitin-binding compound induces the mitochondrial apoptotic pathway through NOXA and BIM upregulation.

Cristina Moncunill-Massaguer, José Saura-Esteller, Alba Pérez-Perarnau, Claudia Mariela Palmeri, Sonia Núñez-Vázquez, Ana M Cosialls, Diana M González-Gironès, Helena Pomares, Anne Korwitz, Sara Preciado and 6 more

Open access · diamondAbstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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  10. Fluorizoline-induced apoptosis requires prohibitins in nematodes and human cells.Apoptosis : an international journal on programmed cell death · 2021
    Article
  11. Review
  12. SFPH proteins as therapeutic targets for a myriad of diseases.Bioorganic & medicinal chemistry letters · 2020
    Review
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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

16 authors at 5 institutions in 2 countries.

Cristina Moncunill-MassaguerDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
José Saura-EstellerDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Alba Pérez-PerarnauDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Claudia Mariela PalmeriDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Sonia Núñez-VázquezDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Ana M CosiallsDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Diana M González-GironèsDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Helena PomaresDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Anne KorwitzInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Sara PreciadoBarcelona Science Park and CIBER-BBN, Networking Centre on Bioengineering, Biomaterials and Nanomedicine, Barcelona, Spain.
Fernando AlbericioBarcelona Science Park and CIBER-BBN, Networking Centre on Bioengineering, Biomaterials and Nanomedicine, Barcelona, Spain.
Rodolfo LavillaBarcelona Science Park and CIBER-BBN, Networking Centre on Bioengineering, Biomaterials and Nanomedicine, Barcelona, Spain.
Gabriel PonsDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Thomas LangerInstitute for Genetics and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Daniel Iglesias-SerretDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Joan GilDepartament de Ciències Fisiològiques II, Universitat de Barcelona-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Catalunya, Spain.
Universitat de Barcelona · ESInstitut d'Investigació Biomédica de Bellvitge · ESBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESUniversity of Cologne · DEManufacturas Serviplast (Spain) · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously described diaryl trifluorothiazoline compound 1a (hereafter referred to as fluorizoline) as a first-in-class small molecule that induces p53-independent apoptosis in a wide range of tumor cell lines. Fluorizoline directly binds to prohibitin 1 and 2 (PHBs), two proteins involved in the regulation of several cellular processes, including apoptosis. Here we demonstrate that fluorizoline-induced apoptosis is mediated by PHBs, as cells depleted of these proteins are highly resistant to fluorizoline treatment. In addition, BAX and BAK are necessary for fluorizoline-induced cytotoxic effects, thereby proving that apoptosis occurs through the intrinsic pathway. Expression analysis revealed that fluorizoline induced the upregulation of Noxa and Bim mRNA levels, which was not observed in PHB-depleted MEFs. Finally, Noxa(-/-)/Bim(-/-) MEFs and NOXA-downregulated HeLa cells were resistant to fluorizoline-induced apoptosis. All together, these findings show that fluorizoline requires PHBs to execute the mitochondrial apoptotic pathway.

Indexed as

AnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Dose-Response Relationship, DrugDrug Resistance, NeoplasmFibroblastsHeLa CellsHT29 CellsHumansJurkat CellsMembrane ProteinsMiceMitochondriaNeoplasmsAntineoplastic AgentsApoptosis Regulatory ProteinsBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11Membrane ProteinsPHB protein, humanPMAIP1 protein, humanPmaip1 protein, mouseProhibitinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesRepressor ProteinsThiazolesapoptosisBCL-2 family memberscancermitochondriaprohibitins

Identifiers

PMID26497683
PMCPMC4747186
OpenAlexW2261583913

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.