Evidence map›Paper›PMID 32020055›Full record

ArticleOncogene2020

C3a elicits unique migratory responses in immature low-density neutrophils.

Brian E Hsu, Joannie Roy, Jack Mouhanna, Roni F Rayes, LeeAnn Ramsay, Sébastien Tabariès, Matthew G Annis, Ian R Watson, Jonathan D Spicer, Santiago Costantino and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Complement system in tumor growth and metastases.British journal of cancer · 2026
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  9. Cell Trafficking at the Intersection of the Tumor-Immune Compartments.Annual review of biomedical engineering · 2022
    Review
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  11. Inside-Out of Complement in Cancer.Frontiers in immunology · 2022
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  13. 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

11 authors at 2 institutions in 1 country.

Brian E HsuGoodman Cancer Research Centre, McGill University, Montréal, QC, H3A 1A3, Canada.
Joannie RoyResearch Centre, Maisonneuve-Rosemont Hospital, Montréal, QC, H1T 2M4, Canada.
Jack MouhannaDepartment of Surgery, Research Institute of the McGill University Health Center, Montréal, QC, H4A 3J1, Canada.
Roni F RayesDepartment of Surgery, Research Institute of the McGill University Health Center, Montréal, QC, H4A 3J1, Canada.
LeeAnn RamsayGoodman Cancer Research Centre, McGill University, Montréal, QC, H3A 1A3, Canada.
Sébastien TabarièsGoodman Cancer Research Centre, McGill University, Montréal, QC, H3A 1A3, Canada.
Matthew G AnnisGoodman Cancer Research Centre, McGill University, Montréal, QC, H3A 1A3, Canada.
Ian R WatsonGoodman Cancer Research Centre, McGill University, Montréal, QC, H3A 1A3, Canada.
Jonathan D SpicerDepartment of Surgery, Research Institute of the McGill University Health Center, Montréal, QC, H4A 3J1, Canada.
Santiago CostantinoResearch Centre, Maisonneuve-Rosemont Hospital, Montréal, QC, H1T 2M4, Canada.
Peter M SiegelGoodman Cancer Research Centre, McGill University, Montréal, QC, H3A 1A3, Canada. peter.siegel@mcgill.ca.ORCID http://orcid.org/0000-0002-5568-6586
McGill University Health Centre · CAHôpital Maisonneuve-Rosemont · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils represent the immune system's first line of defense and are rapidly recruited into inflamed tissue. In cancer associated inflammation, phenotypic heterogeneity has been ascribed to this cell type, whereby neutrophils can manifest anti- or pro-metastatic functions depending on the cellular/micro-environmental context. Here, we demonstrate that pro-metastatic immature low-density neutrophils (iLDNs) more efficiently accumulate in the livers of mice bearing metastatic lesions compared with anti-metastatic mature high-density neutrophils (HDNs). Transcriptomic analyses reveal enrichment of a migration signature in iLDNs relative to HDNs. We find that conditioned media derived from liver-metastatic breast cancer cells, but not lung-metastatic variants, specifically induces chemotaxis of iLDNs and not HDNs. Chemotactic responses are due to increased surface expression of C3aR in iLDNs relative to HDNs. In addition, we detect elevated secretion of cancer-cell derived C3a from liver-metastatic versus lung-metastatic breast cancer cells. Perturbation of C3a/C3aR signaling axis with either a small molecule inhibitor, SB290157, or reducing the levels of secreted C3a from liver-metastatic breast cancer cells by short hairpin RNAs, can abrogate the chemotactic response of iLDNs both in vitro and in vivo, respectively. Together, these data reveal novel mechanisms through which iLDNs prefentially accumulate in liver tissue harboring metastases in response to tumor-derived C3a secreted from the liver-aggressive 4T1 breast cancer cells.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorCell MovementComplement C3aCulture Media, ConditionedFemaleLiver NeoplasmsMiceMice, Inbred BALB CNeoplasm MetastasisNeutrophilsReceptors, ComplementComplement C3acomplement C3a receptorCulture Media, ConditionedReceptors, Complement

Identifiers

PMID32020055
OpenAlexW3004629638

What OpenQuestion holds

Textmetadata
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.