Evidence map›Paper›PMID 27526676›Full record

ArticleBMC cancer2016

The deficiency of galectin-3 in stromal cells leads to enhanced tumor growth and bone marrow metastasis.

Jonathas Xavier Pereira, Maria Carolina Braga Azeredo, Felipe Sá Martins, Roger Chammas, Felipe Leite Oliveira, Sofia Nascimento Santos, Emerson Soares Bernardes, Márcia Cury El-Cheikh

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 18 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

8 authors at 4 institutions in 1 country.

Jonathas Xavier PereiraPrograma de Pós-Graduação em Anatomia Patológica, Hospital Clementino Fraga Filho, UFRJ, Rio de Janeiro, Brazil.
Maria Carolina Braga AzeredoPrograma de Pós-Graduação em Ciências Morfológicas, ICB, UFRJ, Rio de Janeiro, Brazil.
Felipe Sá MartinsUniversidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Roger ChammasLaboratório de Oncologia Experimental e Instituto do Câncer do Estado de São Paulo, Faculdade de Medicina, São Paulo, Brazil.
Felipe Leite OliveiraLaboratório de Proliferação e Diferenciação Celular, ICB, UFRJ, Rio de Janeiro, RJ, Brazil.
Sofia Nascimento SantosCentro de Radiofarmácia, Instituto de Pesquisas Energéticas e Nucleares (IPEN), São Paulo, Brazil.
Emerson Soares BernardesCentro de Radiofarmácia, Instituto de Pesquisas Energéticas e Nucleares (IPEN), São Paulo, Brazil.
Márcia Cury El-CheikhLaboratório de Proliferação e Diferenciação Celular, ICB, UFRJ, Rio de Janeiro, RJ, Brazil. marcia@histo.ufrj.br.
Instituto de Pesquisas Energéticas e Nucleares · BRUniversidade Federal do Rio de Janeiro · BRHospital Universitário Clementino Fraga Filho · BRInstituto do Câncer do Estado de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGalectin-3 is a multifunctional β-galactoside-binding lectin that once synthesized, is expressed in the nucleus, cytoplasm, cell surface and in the extracellular environment. Because of its unique structure, galectin-3 can oligomerize forming lattice upon binding to multivalent oligossacharides and influence several pathologic events such as tumorigenesis, invasion and metastasis.

methodsIn our study, balb/c Lgals3+/+ and Lgals3-/- female mice were inoculated in the fourth mammary fat pad with 4T1 breast cancer cell line. The primary tumor, inguinal lymph nodes and iliac bone marrow were evaluated 15, 21 and 28 days post-injection. The primary tumor growth was evaluated by measuring the external diameter, internal growth by ultrasound and weight of the excised tumor. The presence of cancer cells in the draining lymph nodes and iliac crest bone marrow were performed by immunohistochemistry, PCR and clonogenic metastatic assay.

resultsIn this study we demonstrated that the deletion of galectin-3 in the host affected drastically the in vivo growth rate of 4T1 tumors. The primary tumors in Lgals3-/- mice displayed a higher proliferative rate (p < 0,05), an increased necrotic area (p < 0,01) and new blood vessels with a wider lumen in comparison with tumors from Lgals3+/+ mice (P < 0,05). Moreover, we detected a higher number of 4T1-derived metastatic colonies in the lymph nodes and the bone marrow of Lgals3-/- mice (p < 0,05). Additionally, healthy Lgals3-/- control mice presented an altered spatial distribution of CXCL12 in the bone marrow, which may explain at least in part the initial colonization of this organ in Lgals3-/- injected with 4T1 cells.

conclusionsTaken together, our results demonstrate for the first time that the absence of galectin-3 in the host microenvironment favors the growth of the primary tumors, the metastatic spread to the inguinal lymph nodes and bone marrow colonization by metastatic 4T1 tumor cells.

Indexed as

AnimalsBone Marrow NeoplasmsBreast NeoplasmsCell Line, TumorCell ProliferationFemaleGalectin 3Lymph NodesMice, Inbred BALB CNeoplasm TransplantationGalectin 3Lgals3 protein, mouse4T1 breast carcinomaBone marrow metastasisCXCR4/CXCL12 axisGalectin-3

Identifiers

PMID27526676
PMCPMC4986277
OpenAlexW2509114986

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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.