Evidence map›Paper›PMID 33298879›Full record

ArticleCell death discovery2020

Macrophages produce and functionally respond to interleukin-34 in colon cancer.

Eleonora Franzè, Federica Laudisi, Antonio Di Grazia, Martin Marônek, Vittoria Bellato, Giuseppe Sica, Giovanni Monteleone

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

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  8. The roles of tissue resident macrophages in health and cancer.Experimental hematology & oncology · 2024
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  12. PET/CT imaging of CSF1R in a mouse model of tuberculosis.European journal of nuclear medicine and molecular imaging · 2022
    Article
  13. Article
  14. Article
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  16. Targeting IL-34/MCSF-1R Axis in Colon Cancer.Frontiers in immunology · 2022
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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

7 authors at 2 institutions in 2 countries.

Eleonora FranzèDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Federica LaudisiDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Antonio Di GraziaDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Martin MarônekInstitute of Molecular Biomedicine, Faculty of Medicine, Comenius University in Bratislava, Bratislava, Slovakia.
Vittoria BellatoDepartment of Surgery, University "TOR VERGATA" of Rome, Rome, Italy.
Giuseppe SicaDepartment of Surgery, University "TOR VERGATA" of Rome, Rome, Italy.
Giovanni MonteleoneDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy. Gi.Monteleone@Med.uniroma2.it.
University of Rome Tor Vergata · ITComenius University Bratislava · SK

Funding

Associazione Italiana per la Ricerca sul Cancro (Italian Association for Cancer Research) IG2016-19223
6 · The paper itself

Abstract

In colorectal cancer (CRC), macrophages represent a major component of the tumor mass and exert mostly functions promoting tumor cell survival, proliferation, and dissemination. Interleukin-34 (IL-34) is a cytokine overproduced by colon cancer (CRC) cells and supposed to make a valid contribution to the growth and diffusion of CRC cells. The biological functions of IL-34 are mediated by the macrophage colony-stimulating factor receptor (M-CSFR-1), which controls monocyte/macrophage differentiation, growth, and survival. We here investigated whether, in CRC, tumor-associated macrophages (TAMs) express M-CSFR-1 and functionally respond to IL-34. By flow-cytometry analysis of tumor-infiltrating cells (TICs) and lamina propria mononuclear cells (LPMCs) isolated from normal, adjacent mucosa of CRC patients, we showed that CD68/HLA-DRII-expressing TICs and LPMCs expressed M-CSFR-1. Both these cell types produced IL-34 even though the expression of the cytokine was more pronounced in TICs as compared to normal LPMCs. Moreover, in CRC samples, there was a positive correlation between IL-34-producing cells and CD68-positive cells. Stimulation of LPMCs and TICs with IL-34 resulted in enhanced expression of CD163 and CD206, two markers of type II-polarized macrophages, and this was evident at both RNA and protein level. In the same cell cultures, IL-34 stimulated expression and production of IL-6, a cytokine known to promote CRC cell growth and diffusion. Finally, knockdown of IL-34 in TICs with specific antisense oligonucleotides with: a specific antisesne oligonucleotide decreased IL-6 production and the number of TAMs producing this cytokine. This is the first to show a positive role of IL-34 in the control of TAMs in CRC, further supporting the notion that IL-34 sustains colon tumorigenesis.

Identifiers

PMID33298879
PMCPMC7644720
OpenAlexW3097021382

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.