Evidence map›Paper›PMID 24421272›Full record

ArticleCancer medicine2014

Galectin-3 disruption impaired tumoral angiogenesis by reducing VEGF secretion from TGFβ1-induced macrophages.

Camila Maria Longo Machado, Luciana Nogueira Sousa Andrade, Verônica Rodrigues Teixeira, Fabrício Falconi Costa, Camila Morais Melo, Sofia Nascimento dos Santos, Suely Nonogaki, Fu-Tong Liu, Emerson Soares Bernardes, Anamaria Aranha Camargo and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026
    Review
  3. International journal of molecular sciences · 2025
    Article
  4. Galectins and Liver Diseases.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. Melanoma stimulates the proteolytic activity of HaCaT keratinocytes.Cell communication and signaling : CCS · 2022
    Article
  9. MG-International journal of molecular sciences · 2022
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. 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 6 institutions in 3 countries.

Camila Maria Longo MachadoLaboratório de Oncologia Experimental-LIM24, Departamento de Radiologia e Oncologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil; Depto. de Radiologia e Oncologia, Centro de Investigação Translacional em Oncologia, Instituto do Câncer do Estado de São Paulo, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil; Laboratório de Investigação Médica Radioisotopos-LIM/43, Departamento de Radiologia e Oncologia, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.
Luciana Nogueira Sousa Andrade
Verônica Rodrigues Teixeira
Fabrício Falconi Costa
Camila Morais Melo
Sofia Nascimento dos Santos
Suely Nonogaki
Fu-Tong Liu
Emerson Soares Bernardes
Anamaria Aranha Camargo
Roger Chammas
Instituto do Câncer do Estado de São Paulo · BRUniversidade de São Paulo · BRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRInstitute of Biomedical Sciences, Academia Sinica · TWInstituto Adolfo Lutz · BRNorthwestern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to study the role of galectin-3 in tumor angiogenesis associated with tumor-associated macrophages (TAM) and tumor parenchyma, the galectin-3 expression was reconstituted in Tm1 melanoma cell line that lacks this protein. Galectin-3-expressing cells (Tm1G3) and mock-vector transfected cells (Tm1N3) were injected into wild-type (WT) and galectin-3 knockout (KO) C57Bl/6 mice. Tumors originated from Tm1G3 were larger in tumor volume with enlarged functional vessels, decreased necrotic areas, and increased vascular endothelial growth factor (VEGF) protein levels. Galectin-3-nonexpressing-cells injected into WT and KO showed increased levels of transforming growth factor beta 1 (TGFβ1) and, in WT animals this feature was also accompanied by increased VEGFR2 expression and its phosphorylation. In KO animals, tumors derived from galectin-3-expressing cells were infiltrated by CD68(+)-cells, whereas in tumors derived from galectin-3-nonexpressing-cells, CD68(+) cells failed to infiltrate tumors and accumulated in the periphery of the tumor mass. In vitro studies showed that Tm1G3 secreted more VEGF than Tm1N3 cells. In the latter case, TGFβ1 induced VEGF production. Basal secretion of VEGF was higher in WT-bone marrow-derived macrophages (BMDM) than in KO-BMDM. TGFβ1 induced secretion of VEGF only in WT-BMDM. Tm1G3-induced tumors had the Arginase I mRNA increased, which upregulated alternative macrophage (M2)/TAM induction. M2 stimuli, such as interleukin-4 (IL4) and TGFβ1, increased Arginase I protein levels and galectin-3 expression in WT- BMDM, but not in cells from KO mice. Hence, we report that galectin-3 disruption in tumor stroma and parenchyma decreases angiogenesis through interfering with the responses of macrophages to the interdependent VEGF and TGFβ1 signaling pathways.

Indexed as

AnimalsDNA MethylationGalectin 3HumansMacrophagesMaleMelanomaMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicPromoter Regions, GeneticTransforming Growth Factor beta1Tumor MicroenvironmentVascular Endothelial Growth Factor AGalectin 3Transforming Growth Factor beta1Vascular Endothelial Growth Factor AAngiogenesisgalectin-3melanomatumor microenvironment

Identifiers

PMID24421272
PMCPMC3987071
OpenAlexW2005276971

What OpenQuestion holds

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LicenceCC BY
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.