Evidence map›Paper›PMID 36522309›Full record

ArticleCell death & disease2022

TRAIL receptors promote constitutive and inducible IL-8 secretion in non-small cell lung carcinoma.

Francesca Favaro, Fedra Luciano-Mateo, Joaquim Moreno-Caceres, Miguel Hernández-Madrigal, Demi Both, Chiara Montironi, Franziska Püschel, Ernest Nadal, Eric Eldering, Cristina Muñoz-Pinedo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Interleukin-8 in health and disease.Molecular biomedicine · 2026
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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

10 authors at 3 institutions in 2 countries.

Francesca FavaroPreclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.ORCID 0000-0002-4184-140X
Fedra Luciano-Mateo *Preclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.
Joaquim Moreno-Caceres *Preclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.ORCID 0000-0002-4166-9419
Miguel Hernández-MadrigalPreclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.
Demi BothPreclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.
Chiara MontironiAmsterdam UMC location University of Amsterdam, Department of Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.ORCID 0000-0003-0753-231X
Franziska PüschelPreclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.
Ernest NadalPreclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain.ORCID 0000-0002-9674-5554
Eric ElderingAmsterdam UMC location University of Amsterdam, Department of Experimental Immunology, Meibergdreef 9, Amsterdam, The Netherlands.
Cristina Muñoz-PinedoPreclinical and Experimental Research in Thoracic Tumors (PReTT), Molecular Mechanisms and Experimental Therapy in Oncology Program (Oncobell), Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, 08908, Barcelona, Spain. cmunoz@idibell.cat.ORCID 0000-0002-9120-664X
Institut d'Investigació Biomédica de Bellvitge · ESAmsterdam University Medical Centers · NLOncode Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-8 (IL-8/CXCL8) is a pro-angiogenic and pro-inflammatory chemokine that plays a role in cancer development. Non-small cell lung carcinoma (NSCLC) produces high amounts of IL-8, which is associated with poor prognosis and resistance to chemo-radio and immunotherapy. However, the signaling pathways that lead to IL-8 production in NSCLC are unresolved. Here, we show that expression and release of IL-8 are regulated autonomously by TRAIL death receptors in several squamous and adenocarcinoma NSCLC cell lines. NSCLC constitutively secrete IL-8, which could be further enhanced by glucose withdrawal or by treatment with TRAIL or TNFα. In A549 cells, constitutive and inducible IL-8 production was dependent on NF-κB and MEK/ERK MAP Kinases. DR4 and DR5, known regulators of these signaling pathways, participated in constitutive and glucose deprivation-induced IL-8 secretion. These receptors were mainly located intracellularly. While DR4 signaled through the NF-κB pathway, DR4 and DR5 both regulated the ERK-MAPK and Akt pathways. FADD, caspase-8, RIPK1, and TRADD also regulated IL-8. Analysis of mRNA expression data from patients indicated that IL-8 transcripts correlated with TRAIL, DR4, and DR5 expression levels. Furthermore, TRAIL receptor expression levels also correlated with markers of angiogenesis and neutrophil infiltration in lung squamous carcinoma and adenocarcinoma. Collectively, these data suggest that TRAIL receptor signaling contributes to a pro-tumorigenic inflammatory signature associated with NSCLC.

Indexed as

AdenocarcinomaCarcinoma, Non-Small-Cell LungLung NeoplasmsApoptosisCell Line, TumorGlucoseHumansInterleukin-8NF-kappa BReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandGlucoseInterleukin-8NF-kappa BReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID36522309
PMCPMC9755151
OpenAlexW4311542544

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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.