Evidence map›Paper›PMID 26330543›Full record

ArticleMolecular & cellular proteomics : MCP2015

Molecular Consequences of Proprotein Convertase 1/3 (PC1/3) Inhibition in Macrophages for Application to Cancer Immunotherapy: A Proteomic Study.

Marie Duhamel, Franck Rodet, Nadira Delhem, Fabien Vanden Abeele, Firas Kobeissy, Serge Nataf, Laurent Pays, Roxanne Desjardins, Hugo Gagnon, Maxence Wisztorski and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Self or nonself: end of a dogma?Frontiers in immunology · 2025
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  19. PROPROTEIN CONVERTASE 1/3 DEFICIENCY WITH PELVIC EWING SARCOMA.Acta endocrinologica (Bucharest, Romania : 2005)
    Article
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

13 authors at 8 institutions in 4 countries.

Marie DuhamelFrom the ‡Inserm U-1192, Laboratoire de Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM), Université Lille 1, Cité Scientifique, 59655 Villeneuve D'Ascq, France;
Franck RodetFrom the ‡Inserm U-1192, Laboratoire de Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM), Université Lille 1, Cité Scientifique, 59655 Villeneuve D'Ascq, France;
Nadira Delhem§Institut de Biologie de Lille, UMR 8161 CNRS, Institut Pasteur de Lille, Université Lille 1, Lille, France;
Fabien Vanden Abeele¶Inserm U-1003, Equipe labellisée par la Ligue Nationale contre le cancer, Laboratory of Excellence, Ion Channels Science and Therapeutics, Université Lille 1, Cité Scientifique, 59655 Villeneuve d'Ascq, France;
Firas Kobeissy‖Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut;
Serge Nataf**Inserm U-1060, CarMeN Laboratory, Banque de Tissus et de Cellules des Hospices Civils de Lyon, Université Lyon-1;
Laurent Pays**Inserm U-1060, CarMeN Laboratory, Banque de Tissus et de Cellules des Hospices Civils de Lyon, Université Lyon-1;
Roxanne Desjardins‡‡Institut de Pharmacologie, Département de Chirurgie/Service d'Urologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, J1H 5N4 Québec, Canada;
Hugo Gagnon§§PhenoSwitch Bioscience Inc. 3001 12 Ave Nord, Sherbrooke, Qc, Canada, J1H 5N4.
Maxence WisztorskiFrom the ‡Inserm U-1192, Laboratoire de Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM), Université Lille 1, Cité Scientifique, 59655 Villeneuve D'Ascq, France;
Isabelle FournierFrom the ‡Inserm U-1192, Laboratoire de Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM), Université Lille 1, Cité Scientifique, 59655 Villeneuve D'Ascq, France;
Robert Day‡‡Institut de Pharmacologie, Département de Chirurgie/Service d'Urologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, J1H 5N4 Québec, Canada;
Michel SalzetFrom the ‡Inserm U-1192, Laboratoire de Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM), Université Lille 1, Cité Scientifique, 59655 Villeneuve D'Ascq, France; michel.salzet@univ-lille1.fr.ORCID http://orcid.org/0000-0003-4318-0817
Protéomique, Réponse Inflammatoire et Spectrométrie de Masse · FRInserm · FRUniversité de Sherbrooke · CAAmerican University of Beirut · LBCentre National de la Recherche Scientifique · FRLa Ligue Contre le Cancer · FRLyon College · USUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages provide the first line of host immune defense. Their activation triggers the secretion of pro-inflammatory cytokines and chemokines recruiting other immune cells. In cancer, macrophages present an M2 anti-inflammatory phenotype promoting tumor growth. In this way, strategies need to be develop to reactivate macrophages. Previously thought to be expressed only in cells with a neural/neuroendocrine phenotype, the proprotein convertase 1/3 has been shown to also be expressed in macrophages and regulated as a function of the Toll-like receptor immune response. Here, we investigated the intracellular impact of the down-regulation of the proprotein convertase 1/3 in NR8383 macrophages and confirmed the results on macrophages from PC1/3 deficient mice. A complete proteomic study of secretomes and intracellular proteins was undertaken and revealed that inhibition of proprotein convertase 1/3 orient macrophages toward an M1 activated phenotype. This phenotype is characterized by filopodial extensions, Toll-like receptor 4 MyD88-dependent signaling, calcium entry augmentation and the secretion of pro-inflammatory factors. In response to endotoxin/lipopolysaccharide, these intracellular modifications increased, and the secreted factors attracted naïve T helper lymphocytes to promote the cytotoxic response. Importantly, the application of these factors onto breast and ovarian cancer cells resulted in a decrease viability or resistance. Under inhibitory conditions using interleukin 10, PC1/3-knockdown macrophages continued to secrete inflammatory factors. These data indicate that targeted inhibition of proprotein convertase 1/3 could represent a novel type of immune therapy to reactivate intra-tumoral macrophages.

Indexed as

AnimalsCalciumCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell LineCell Line, TumorCytokinesGene Expression RegulationHumansImmunotherapyKiller Cells, NaturalLipopolysaccharidesMacrophages, AlveolarMacrophages, PeritonealMiceMice, KnockoutCalciumCytokinesLipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88Proprotein Convertase 1RNA, Small InterferingTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID26330543
PMCPMC4638031
OpenAlexW2101175892

What OpenQuestion holds

Textmetadata
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.