Evidence map›Paper›PMID 22918244›Full record

ArticleCell cycle (Georgetown, Tex.)2012

Independent transcriptional reprogramming and apoptosis induction by cisplatin.

Lorenzo Galluzzi, Ilio Vitale, Laura Senovilla, Tobias Eisenberg, Didac Carmona-Gutierrez, Erika Vacchelli, Thomas Robert, Hugues Ripoche, Nora Jägemann, Caroline Paccard and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. 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
2.1field-weighted citation impact, top 13% 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, 30 citations in OpenAlex.

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  11. Hesperidin from Citrus seed induces human hepatocellular carcinoma HepG2 cell apoptosis via both mitochondrial and death receptor pathways.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
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  15. Lipids and cell death in yeast.FEMS yeast research · 2014
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 3 countries.

Lorenzo GalluzziUniversité Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France.
Ilio Vitale
Laura Senovilla
Tobias Eisenberg
Didac Carmona-Gutierrez
Erika Vacchelli
Thomas Robert
Hugues Ripoche
Nora Jägemann
Caroline Paccard
Nicolas Servant
Philippe Hupé
Vladimir Lazar
Philippe Dessen
Emmanuel Barillot
Hans Zischka
Frank Madeo
Guido Kroemer
Inserm · FRUniversité Paris-Sud · FRUniversity of Graz · ATCentre National de la Recherche Scientifique · FRDélégation Paris 5 · FRHelmholtz Zentrum München · DEInstitut Gustave Roussy · FR

Funding

Austrian Science Fund FWF P 23490Austrian Science Fund FWF P 24381Austrian Science Fund FWF W 1226
6 · The paper itself

Abstract

Neither the molecular mechanisms whereby cancer cells intrinsically are or become resistant to the DNA-damaging agent cisplatin nor the signaling pathways that account for cisplatin cytotoxicity have thus far been characterized in detail. In an attempt to gain further insights into the molecular cascades elicited by cisplatin (leading to resistance or underpinning its antineoplastic properties), we comparatively investigated the ability of cisplatin, C2-ceramide and cadmium dichloride, alone or in the presence of an array of mitochondrion-protective agents, to trigger the permeabilization of purified mitochondria. In addition, we compared the transcriptional response triggered by cisplatin, C2-ceramide and cadmium dichloride in non-small cell lung carcinoma A549 cells. Finally, we assessed the capacity of cisplatin, C2-ceramide and cadmium dichloride to reduce the clonogenic potential of a battery of yeast strains lacking proteins involved in the regulation of cell death, DNA damage signaling and stress management. This multipronged experimental approach revealed that cisplatin elicits signaling pathways that are for the most part "private," i.e., that manifest limited overlap with the molecular cascades ignited by other inducers of mitochondrial apoptosis, and triggers apoptosis mainly in a transcription-independent fashion. Indeed, bona fide cisplatin-response modifiers that we have recently identified by a functional genome-wide siRNA screen are either not transcriptionally regulated during cisplatin-induced cell death or their transcriptional modulation reflects the activation of an adaptive response promoting cisplatin resistance.

Indexed as

AnimalsApoptosisCadmium ChlorideCell Line, TumorCellular ReprogrammingCeramidesCisplatinGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockout TechniquesHumansMitochondria, LiverPermeabilityRatsSaccharomyces cerevisiaeTranscription, GeneticCadmium ChlorideCeramidesCisplatin

Identifiers

PMID22918244
PMCPMC3466557
OpenAlexW2059601988

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.