Evidence map›Paper›PMID 29445180›Full record

ArticleNature communications2018

Myeloid-derived interleukin-1β drives oncogenic KRAS-NF-κΒ addiction in malignant pleural effusion.

Antonia Marazioti, Ioannis Lilis, Malamati Vreka, Hara Apostolopoulou, Argyro Kalogeropoulou, Ioanna Giopanou, Georgia A Giotopoulou, Anthi C Krontira, Marianthi Iliopoulou, Nikolaos I Kanellakis and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2018. 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
4.2field-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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
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  4. Assessment of Angiogenic Properties of Malignant Pleural Effusion (MPE) Fluid.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
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  19. Article
  20. [Latest Progress of Intraoperative Pleural Lavage Cytology in Lung Cancer Surgery].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2018
    Review
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

19 authors at 3 institutions in 4 countries.

Antonia MaraziotiDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece. amarazioti@upatras.gr.
Ioannis LilisDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Malamati VrekaDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Hara ApostolopoulouDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Argyro KalogeropoulouStem Cell Biology Laboratory, Department of Physiology, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Ioanna GiopanouDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Georgia A GiotopoulouDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Anthi C KrontiraDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Marianthi IliopoulouDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Nikolaos I KanellakisDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Theodora AgaliotiDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Anastasios D GiannouDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Celestial Jones-ParisDivision of Allergy, Pulmonary and Critical Care, Department of Internal Medicine, Vanderbilt University School of Medicine, T-1218 MCN, Nashville, TN, 37232-2650, USA.
Yoichiro IwakuraResearch Institute for Biomedical Sciences, Tokyo University of Science, Tokyo, Chiba, 278-0022, Japan.ORCID http://orcid.org/0000-0002-9934-5775
Dimitrios KardamakisDepartment of Radiation Oncology and Stereotactic Radiotherapy, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Timothy S BlackwellDivision of Allergy, Pulmonary and Critical Care, Department of Internal Medicine, Vanderbilt University School of Medicine, T-1218 MCN, Nashville, TN, 37232-2650, USA.
Stavros TaravirasStem Cell Biology Laboratory, Department of Physiology, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Magda SpellaDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece.
Georgios T StathopoulosDepartment of Physiology, Laboratory for Molecular Respiratory Carcinogenesis, Faculty of Medicine, University of Patras, 26504, Rio, Achaia, Greece. gstathop@upatras.gr.ORCID http://orcid.org/0000-0002-9215-6461
University of Patras · GRVanderbilt University · USTokyo University of Science · JP

Funding

European Research Council
6 · The paper itself

Abstract

Malignant pleural effusion (MPE) is a frequent metastatic manifestation of human cancers. While we previously identified KRAS mutations as molecular culprits of MPE formation, the underlying mechanism remained unknown. Here, we determine that non-canonical IKKα-RelB pathway activation of KRAS-mutant tumor cells mediates MPE development and this is fueled by host-provided interleukin IL-1β. Indeed, IKKα is required for the MPE-competence of KRAS-mutant tumor cells by activating non-canonical NF-κB signaling. IL-1β fuels addiction of mutant KRAS to IKKα resulting in increased CXCL1 secretion that fosters MPE-associated inflammation. Importantly, IL-1β-mediated NF-κB induction in KRAS-mutant tumor cells, as well as their resulting MPE-competence, can only be blocked by co-inhibition of both KRAS and IKKα, a strategy that overcomes drug resistance to individual treatments. Hence we show that mutant KRAS facilitates IKKα-mediated responsiveness of tumor cells to host IL-1β, thereby establishing a host-to-tumor signaling circuit that culminates in inflammatory MPE development and drug resistance.

Indexed as

Genes, rasAnimalsCell Line, TumorChemokine CXCL1FemaleHumansI-kappa B KinaseInterleukin-1betaMaleMiceMice, Inbred C57BLMutationMyeloid CellsNF-kappa BPleural Effusion, MalignantReceptors, Interleukin-1Chemokine CXCL1Cxcl1 protein, mouseI-kappa B KinaseInterleukin-1betaNF-kappa BReceptors, Interleukin-1

Identifiers

PMID29445180
PMCPMC5813197
OpenAlexW2805413615

What OpenQuestion holds

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LicenceCC BY
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.