Evidence map›Paper›PMID 29423057›Full record

ArticleOncotarget2018

Interleukin-34 sustains pro-tumorigenic signals in colon cancer tissue.

Eleonora Franzè, Vicenzo Dinallo, Angela Rizzo, Martina Di Giovangiulio, Gerolamo Bevivino, Carmine Stolfi, Flavio Caprioli, Alfredo Colantoni, Angela Ortenzi, Antonio Di Grazia and 4 more

Abstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

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  11. Targeting IL-34/MCSF-1R Axis in Colon Cancer.Frontiers in immunology · 2022
    Review
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  14. Article
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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

14 authors.

Eleonora FranzèDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Vicenzo DinalloDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Angela RizzoDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Martina Di GiovangiulioDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Gerolamo BevivinoDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Carmine StolfiDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Flavio CaprioliDepartment of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Alfredo ColantoniDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Angela OrtenziDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Antonio Di GraziaDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.
Giuseppe SicaDepartment of Surgery, University "TOR VERGATA" of Rome, Rome, Italy.
Pier Paolo SileriDepartment of Surgery, University "TOR VERGATA" of Rome, Rome, Italy.
Piero RossiDepartment of Surgery, University "TOR VERGATA" of Rome, Rome, Italy.
Giovanni MonteleoneDepartment of Systems Medicine, University of Rome "TOR VERGATA", Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-34 (IL-34), a cytokine produced by a wide range of cells, binds to the macrophage colony-stimulating factor receptor (M-CSFR-1) and receptor-type protein-tyrosine phosphatase zeta (PTP-z) and controls myeloid cell differentiation, proliferation and survival. various types of cancers over-express IL-34 but the role of the cytokine in colorectal cancer (CRC) remains unknown. We here investigated the expression and functional role of IL-34 in CRC. A more pronounced expression of IL-34 was seen in CRC samples as compared to matched normal/benign colonic samples and this occurred at both RNA and protein level. Immunohistochemical analysis of CRC tissue samples showed that both cancer cells and lamina propria mononuclear cells over-expressed IL-34. Additionally, CRC cells expressed both M-CSFR-1 and PTP-z, thus suggesting that CRC cells can be responsive to IL-34. Indeed, stimulation of DLD-1 cancer cells with IL-34, but not with MSCF1, enhanced the cell proliferation and cell invasion without affecting cell survival. Analysis of intracellular signals underlying the mitogenic effect of IL-34 revealed that the cytokine enhanced activation of ERK1/2 and pharmacologic inhibition of ERK1/2 abrogated IL-34-driven cell proliferation. Consistently, IL-34 knockdown in HT-29 cells with a specific IL-34 antisense oligonucleotide reduced ERK1/2 activation, cell proliferation and enhanced the susceptibility of cells to Oxaliplatin-induced death. This is the first study showing up-regulation of IL-34 in CRC and suggesting a role for this cytokine in colon tumorigenesis.

Indexed as

colorectal cancerERK 1/2IL-34M-CSF-1tumorigenesis

Identifiers

PMID29423057
PMCPMC5790474

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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.