Evidence map›Paper›PMID 26657115›Full record

ArticleOncotarget2015

IL-27 induces the expression of IDO and PD-L1 in human cancer cells.

Grazia Carbotti, Gaia Barisione, Irma Airoldi, Delia Mezzanzanica, Marina Bagnoli, Simone Ferrero, Andrea Petretto, Marina Fabbi, Silvano Ferrini

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 94 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 6 pooled it
2.9field-weighted citation impact, top 9% 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

94 citing papers in PubMed, 6 syntheses or guidelines pooled it, 142 citations in OpenAlex.

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  7. Transcriptomic Correlates of Tumor Cell PD-L1 Expression and Response to Nivolumab Monotherapy in Metastatic Clear Cell Renal Cell Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
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34 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

9 authors at 3 institutions in 1 country.

Grazia CarbottiDepartment of Integrated Oncological Therapies, IRCCS AOU San Martino-IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
Gaia BarisioneDepartment of Integrated Oncological Therapies, IRCCS AOU San Martino-IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
Irma AiroldiLaboratory of Oncology, Istituto Giannina Gaslini, Genoa, Italy.
Delia MezzanzanicaDepartment of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Marina BagnoliDepartment of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy.
Simone FerreroDepartment of Surgery, Unit of Obstetrics and Gynaecology, IRCCS AOU San Martino-IST Istituto Nazionale per la Ricerca sul Cancro, and DINOGMI, University of Genoa Genoa, Italy.
Andrea PetrettoCore Facilities, Istituto Giannina Gaslini, Genoa, Italy.
Marina FabbiDepartment of Integrated Oncological Therapies, IRCCS AOU San Martino-IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
Silvano FerriniDepartment of Integrated Oncological Therapies, IRCCS AOU San Martino-IST Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy.
Ospedale Policlinico San Martino · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITIstituto Giannina Gaslini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-27 is a member of the IL-12 family that is produced by macrophages and dendritic cells. IL-27 inhibits the growth and invasiveness of different cancers and therefore represents a potential anti-tumor agent. By contrast, it may exert immune-regulatory properties in different biological systems. We reported that IL-27 induces the expression of the IL-18 inhibitor IL-18BP, in human Epithelial Ovarian Cancer (EOC) cells, thus potentially limiting the immune response. Here, we tested whether IL-27 may modulate other immune-regulatory molecules involved in EOC progression, including Indoleamine 2,3-dioxygenase (IDO) and Programmed Death-Ligand (PD-L)1. IDO and PD-L1 were not constitutively expressed by EOC cells in vitro, but IL-27 increased their expression through STAT1 and STAT3 tyrosine phosphorylation. Differently, cells isolated from EOC ascites showed constitutive activation of STAT1 and STAT3 and IDO expression. These findings, together with the expression of IL-27 in scattered leukocytes in EOC ascites and tissues, suggest a potential role of IL-27 in immune-regulatory networks of EOC. In addition, IL-27 induced IDO or PD-L1 expression in monocytes and in human PC3 prostate and A549 lung cancer cells. A current paradigm in tumor immunology is that tumor cells may escape from immune control due to "adaptive resistance" mediated by T cell-secreted IFN-γ, which induces PD-L1 and IDO expression in tumor cells. Our present data indicate that also IL-27 has similar activities and suggest that the therapeutic use of IL-27 as anti-cancer agent may have dual effects, in some tumors.

Indexed as

B7-H1 AntigenBlotting, WesternCarcinoma, Ovarian EpithelialCell Line, TumorFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansImmunohistochemistryIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukinsNeoplasms, Glandular and EpithelialOvarian NeoplasmsPolymerase Chain ReactionRNA, Small InterferingTransfectionB7-H1 AntigenCD274 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukinsMYDGF protein, humanRNA, Small InterferingIDOIL-27Immune responseImmunityImmunology and Microbiology SectionPD-L1STAT

Identifiers

PMID26657115
PMCPMC4791231
OpenAlexW2193297874

What OpenQuestion holds

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LicenceCC BY
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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.