Evidence map›Paper›PMID 23644655›Full record

ArticleOncogene2014

Macrophages stimulate gastric and colorectal cancer invasion through EGFR Y(1086), c-Src, Erk1/2 and Akt phosphorylation and smallGTPase activity.

A P Cardoso, M L Pinto, A T Pinto, M I Oliveira, M T Pinto, R Gonçalves, J B Relvas, C Figueiredo, R Seruca, A Mantovani and 3 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.3field-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

78 citing papers in PubMed, 120 citations in OpenAlex.

  1. Review
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  8. Review
  9. Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025
    Review
  10. Review
  11. Myeloid cells meet CD8Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
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  14. Article
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18 more citing papers are in PubMed but not listed here.

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

13 authors at 4 institutions in 3 countries.

A P Cardoso1] Instituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal [2] Faculdade de Engenharia, Universidade do Porto, Porto, Portugal.
M L Pinto1] Instituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal [2] Instituto Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal.
A T Pinto1] Instituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal [2] Faculdade de Engenharia, Universidade do Porto, Porto, Portugal.
M I OliveiraInstituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal.
M T PintoInstituto de Patologia e Imunologia Molecular da Universidade do Porto, Porto, Portugal.
R GonçalvesInstituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal.
J B Relvas1] Instituto de Biologia Celular e Molecular, Universidade do Porto, Porto, Portugal [2] Departamento de Biologia Experimental, Faculdade de Medicina, Universidade do Porto, Porto, Portugal.
C Figueiredo1] Instituto de Patologia e Imunologia Molecular da Universidade do Porto, Porto, Portugal [2] Departmento de Patologia e Oncologia, Faculdade de Medicina, Universidade do Porto, Porto, Portugal.
R Seruca1] Instituto de Patologia e Imunologia Molecular da Universidade do Porto, Porto, Portugal [2] Departmento de Patologia e Oncologia, Faculdade de Medicina, Universidade do Porto, Porto, Portugal.
A Mantovani1] Humanitas Clinical and Research Center, Rozzano, Italy [2] BIOMETRA Department, University of Milan, Milan, Italy.
M MareelLaboratory of Experimental Cancerology, Ghent University Hospital, Ghent, Belgium.
M A Barbosa1] Instituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal [2] Instituto Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal.
M J Oliveira1] Instituto de Engenharia Biomédica, Universidade do Porto, Porto, Portugal [2] Departmento de Patologia e Oncologia, Faculdade de Medicina, Universidade do Porto, Porto, Portugal.
Universidade do Porto · PTIPO Porto · PTGhent University Hospital · BEHumanitas University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interactions between cancer cells and their microenvironment are crucial for malignant progression, as they modulate invasion-related activities. Tumor-associated macrophages are generally considered allies in the process of tumor progression in several types of cancer, although their role on gastric and colorectal carcinomas is still poorly understood. In this report, we studied the influence of primary human macrophages on gastric and colorectal cancer cells, considering invasion, motility/migration, proteolysis and activated intracellular signaling pathways. We demonstrated that macrophages stimulate cancer cell invasion, motility and migration, and that these effects depend on matrix metalloproteinase (MMP) activity and on the activation of epidermal growth factor receptor (EGFR) (at the residue Y(1086)), PLC-γ (phospholipase C-gamma) and Gab1 (GRB2-associated binding protein-1), as evidenced by siRNA (small interference RNA) experiments. Epidermal growth factor (EGF)-immunodepletion impaired macrophage-mediated cancer cell invasion and motility, suggesting that EGF is the pro-invasive and pro-motile factor produced by macrophages. Macrophages also induced gastric and colorectal cancer cell phosphorylation of Akt, c-Src and ERK1/2, and led to an increase of RhoA and Cdc42 activity. Interestingly, whereas macrophage-mediated cancer cell c-Src and ERK1/2 phosphorylation occurred downstream EGFR activation, Akt phosphorylation seems to be a parallel event, taking place in an EGFR-independent manner. The involvement of EGF, EGFR-downstream signaling partners and MMPs in macrophage-mediated invasion provides novel insights into the molecular crosstalk established between cancer cells and macrophages, opening new perspectives for the design of new and more efficient therapeutic strategies to counteract cancer cell invasion.

Indexed as

Blotting, WesternCaco-2 CellsCell Line, TumorCell MovementCells, CulturedCoculture TechniquesColorectal NeoplasmsErbB ReceptorsHumansMacrophagesMatrix MetalloproteinasesMicroscopy, ConfocalMicroscopy, FluorescenceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neoplasm InvasivenessErbB ReceptorsMAPK1 protein, humanMatrix MetalloproteinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktProto-Oncogene Proteins pp60(c-src)rho GTP-Binding ProteinsTyrosine

Identifiers

PMID23644655
OpenAlexW1970030280

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.