Evidence map›Paper›PMID 29212030›Full record

ArticleCell reports2017

Loss of Caveolin-1 in Metastasis-Associated Macrophages Drives Lung Metastatic Growth through Increased Angiogenesis.

Ward Celus, Giusy Di Conza, Ana Isabel Oliveira, Manuel Ehling, Bruno M Costa, Mathias Wenes, Massimiliano Mazzone

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 51 citations in OpenAlex.

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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.

Ward CelusLab of Tumor Inflammation and Angiogenesis, Center for Cancer Biology (CCB), VIB, 3000 Leuven, Belgium; Lab of Tumor Inflammation and Angiogenesis, Department of Oncology, KU Leuven, 3000 Leuven, Belgium.
Giusy Di ConzaLab of Tumor Inflammation and Angiogenesis, Center for Cancer Biology (CCB), VIB, 3000 Leuven, Belgium; Lab of Tumor Inflammation and Angiogenesis, Department of Oncology, KU Leuven, 3000 Leuven, Belgium.
Ana Isabel OliveiraLab of Tumor Inflammation and Angiogenesis, Center for Cancer Biology (CCB), VIB, 3000 Leuven, Belgium; Lab of Tumor Inflammation and Angiogenesis, Department of Oncology, KU Leuven, 3000 Leuven, Belgium; Life and Health Sciences Research Institute, School of Medicine, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal; ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Campus de Gualtar, 4710-057 Braga, Portugal.
Manuel EhlingLab of Tumor Inflammation and Angiogenesis, Center for Cancer Biology (CCB), VIB, 3000 Leuven, Belgium; Lab of Tumor Inflammation and Angiogenesis, Department of Oncology, KU Leuven, 3000 Leuven, Belgium.
Bruno M CostaLife and Health Sciences Research Institute, School of Medicine, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal; ICVS/3B's-PT Government Associate Laboratory, Braga/Guimarães, Campus de Gualtar, 4710-057 Braga, Portugal.
Mathias WenesLab of Tumor Inflammation and Angiogenesis, Center for Cancer Biology (CCB), VIB, 3000 Leuven, Belgium; Lab of Tumor Inflammation and Angiogenesis, Department of Oncology, KU Leuven, 3000 Leuven, Belgium. Electronic address: mathias.wenes@unil.ch.
Massimiliano MazzoneLab of Tumor Inflammation and Angiogenesis, Center for Cancer Biology (CCB), VIB, 3000 Leuven, Belgium; Lab of Tumor Inflammation and Angiogenesis, Department of Oncology, KU Leuven, 3000 Leuven, Belgium. Electronic address: massimiliano.mazzone@kuleuven.vib.be.
VIB-KU Leuven Center for Cancer Biology · BEUniversity of Minho · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although it is well established that tumor-associated macrophages take part in each step of cancer progression, less is known about the distinct role of the so-called metastasis-associated macrophages (MAMs) at the metastatic site. Previous studies reported that Caveolin-1 (Cav1) has both tumor-promoting and tumor-suppressive functions. However, the role of Cav1 in bone-marrow-derived cells is unknown. Here, we describe Cav1 as an anti-metastatic regulator in mouse models of lung and breast cancer pulmonary metastasis. Among all the recruited inflammatory cell populations, we show that MAMs uniquely express abundant levels of Cav1. Using clodronate depletion of macrophages, we demonstrate that macrophage Cav1 signaling is critical for metastasis and not for primary tumor growth. In particular, Cav1 inhibition does not affect MAM recruitment to the metastatic site but, in turn, favors angiogenesis. We describe a mechanism by which Cav1 in MAMs specifically restrains vascular endothelial growth factor A/vascular endothelial growth factor receptor 1 (VEGF-A/VEGFR1) signaling and its downstream effectors, matrix metallopeptidase 9 (MMP9) and colony-stimulating factor 1 (CSF1).

Indexed as

AnimalsCaveolin 1Lung NeoplasmsMacrophagesMiceMice, KnockoutNeoplasm MetastasisNeovascularization, PathologicSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Caveolin 1Kdr protein, mouseVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2angiogenesisCaveolin-1CSF1macrophagesmetastasisMMP9VEGF-AVEGFR1

Identifiers

PMID29212030
PMCPMC5732321
OpenAlexW2775398146

What OpenQuestion holds

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LicenceCC BY
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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.