Evidence map›Paper›PMID 24464223›Full record

ArticleCell death and differentiation2014

The protein disulfide isomerases PDIA4 and PDIA6 mediate resistance to cisplatin-induced cell death in lung adenocarcinoma.

G Tufo, A W E Jones, Z Wang, J Hamelin, N Tajeddine, D D Esposti, C Martel, C Boursier, C Gallerne, C Migdal and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 138 citations in OpenAlex.

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6 more citing papers are in PubMed but not listed here.

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

15 authors at 4 institutions in 3 countries.

G Tufo1] INSERM UMR-S 769, LabEx LERMIT, Châtenay-Malabry, France [2] Faculté de Pharmacie, Université de Paris-Sud, Châtenay-Malabry, France.
A W E JonesDepartment of Cell and Developmental Biology, University College London, London, UK.
Z Wang1] INSERM UMR-S 769, LabEx LERMIT, Châtenay-Malabry, France [2] Faculté de Pharmacie, Université de Paris-Sud, Châtenay-Malabry, France.
J HamelinAPHP Hôpital P. Brousse, Biochimie et oncogénétique, INSERM U1004, Villejuif, France.
N TajeddineINSERM U848, Institut Gustave Roussy, Université Paris-Sud 11, PR1, 39 rue Camille Desmoulins, Villejuif, France.
D D EspostiAPHP Hôpital P. Brousse, Biochimie et oncogénétique, INSERM U1004, Villejuif, France.
C Martel1] INSERM UMR-S 769, LabEx LERMIT, Châtenay-Malabry, France [2] Faculté de Pharmacie, Université de Paris-Sud, Châtenay-Malabry, France [3] Montreal Heart Institute, Centre de Recherche, Montreal, Quebec, Canada.
C BoursierIFR 141-IPSIT, Châtenay-Malabry, France.
C Gallerne1] INSERM UMR-S 769, LabEx LERMIT, Châtenay-Malabry, France [2] Faculté de Pharmacie, Université de Paris-Sud, Châtenay-Malabry, France.
C Migdal1] Faculté de Pharmacie, Université de Paris-Sud, Châtenay-Malabry, France [2] INSERM U 996, Châtenay-Malabry, France.
C Lemaire1] INSERM UMR-S 769, LabEx LERMIT, Châtenay-Malabry, France [2] Department of Biology, University of Versailles-St Quentin, Versailles, France.
G Szabadkai1] Department of Cell and Developmental Biology, University College London, London, UK [2] Department of Biomedical Sciences, University of Padua, Padua, Italy.
A LemoineAPHP Hôpital P. Brousse, Biochimie et oncogénétique, INSERM U1004, Villejuif, France.
G Kroemer1] INSERM U848, Institut Gustave Roussy, Université Paris-Sud 11, PR1, 39 rue Camille Desmoulins, Villejuif, France [2] Université Paris Descartes/Paris V, Sorbonne Paris Cité, Paris, France [3] Metabolomics Platform, Institut Gustave Roussy, Villejuif, France [4] Equipe 11 labellisée par la Ligue contre le Cancer, Centre de Recherche des Cordeliers, Paris, France [5] Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-HP, 75015 Paris, France.
C Brenner1] INSERM UMR-S 769, LabEx LERMIT, Châtenay-Malabry, France [2] Faculté de Pharmacie, Université de Paris-Sud, Châtenay-Malabry, France.
Inserm · FRUniversité Paris-Sud · FRUniversity College London · GBUniversity of Padua · IT

Funding

Parkinson's UK G-0905Wellcome Trust
6 · The paper itself

Abstract

Intrinsic and acquired chemoresistance are frequent causes of cancer eradication failure. Thus, long-term cis-diaminedichloroplatine(II) (CDDP) or cisplatin treatment is known to promote tumor cell resistance to apoptosis induction via multiple mechanisms involving gene expression modulation of oncogenes, tumor suppressors and blockade of pro-apoptotic mitochondrial membrane permeabilization. Here, we demonstrate that CDDP-resistant non-small lung cancer cells undergo profound remodeling of their endoplasmic reticulum (ER) proteome (>80 proteins identified by proteomics) and exhibit a dramatic overexpression of two protein disulfide isomerases, PDIA4 and PDIA6, without any alteration in ER-cytosol Ca(2+) fluxes. Using pharmacological and genetic inhibition, we show that inactivation of both proteins directly stimulates CDDP-induced cell death by different cellular signaling pathways. PDIA4 inactivation restores a classical mitochondrial apoptosis pathway, while knockdown of PDIA6 favors a non-canonical cell death pathway sharing some necroptosis features. Overexpression of both proteins has also been found in lung adenocarcinoma patients, suggesting a clinical importance of these proteins in chemoresistance.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsApoptosisCell Line, TumorCisplatinDrug Resistance, NeoplasmHumansLung NeoplasmsProtein Disulfide-IsomerasesAntineoplastic AgentsCisplatinPDIA4 protein, humanPDIA6 protein, humanProtein Disulfide-Isomerases

Identifiers

PMID24464223
PMCPMC3978299
OpenAlexW1978505234

What OpenQuestion holds

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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.