Evidence map›Paper›PMID 28767724›Full record

ArticlePloS one2017

β3 integrin expression is required for invadopodia-mediated ECM degradation in lung carcinoma cells.

Rafael Peláez, Xabier Morales, Elizabeth Salvo, Saray Garasa, Carlos Ortiz de Solórzano, Alfredo Martínez, Ignacio M Larrayoz, Ana Rouzaut

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  15. Invadopodia: clearing the way for cancer cell invasion.Annals of translational medicine · 2020
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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 3 institutions in 1 country.

Rafael PeláezDepartment of Oncology, Center for Applied Medical Research CIMA, Pamplona, Spain.ORCID http://orcid.org/0000-0002-4047-6017
Xabier MoralesDepartment of Oncology, Center for Applied Medical Research CIMA, Pamplona, Spain.
Elizabeth SalvoDepartment of Oncology, Center for Applied Medical Research CIMA, Pamplona, Spain.
Saray GarasaDepartment of Oncology, Center for Applied Medical Research CIMA, Pamplona, Spain.
Carlos Ortiz de SolórzanoLaboratory of Preclinical Models and Analytical Tools, Division of Solid Tumors and Biomarkers, Center for Applied Medical Research and CIBERONC, Pamplona, Navarra, Spain.
Alfredo MartínezOncology Area, Center for Biomedical Research of La Rioja, CIBIR, Logroño, Spain.
Ignacio M LarrayozBiomarkers and Molecular Signaling Group, Neurodegenerative Diseases Area, Center for Biomedical Research of La Rioja, CIBIR, Logroño, Spain.
Ana RouzautDepartment of Oncology, Center for Applied Medical Research CIMA, Pamplona, Spain.
Center for Biomedical Research of La Rioja · ESCentro de Investigación Biomédica en Red de Cáncer · ESUniversidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer related deaths are primarily due to tumor metastasis. To facilitate their dissemination to distant sites, cancer cells develop invadopodia, actin-rich protrusions capable of degrading the surrounding extracellular matrix (ECM). We aimed to determine whether β3 integrin participates in invadopodia formed by lung carcinoma cells, based on our previous findings of specific TGF-β induction of β3 integrin dependent metastasis in animal models of lung carcinoma. In this study, we demonstrate that lung carcinoma cells form invadopodia in response to TGF-β exposure. Invadopodia formation and degradation activity is dependent on β3 integrin expression since β3 integrin deficient cells are not able to degrade gelatin-coated surfaces. Even more, transient over-expression of SRC did not restore invadopodia formation in β3 integrin deficient cells. Finally, we observed that blockade of PLC-dependent signaling leads to more intense labeling for β3 integrin in invadopodia. Our results suggest that β3 integrin function, and location, in lung cancer cells are essential for invadopodia formation, and this integrin regulates the activation of different signal pathways necessary for the invasive structure. β3 integrin has been associated with poor prognosis and increased metastasis in several carcinoma types, including lung cancer. Our findings provide new evidence to support the use of targeted therapies against this integrin to combat the onset of metastases.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell AdhesionCell Line, TumorExtracellular MatrixHumansIntegrin beta3Lung NeoplasmsNeoplasm MetastasisPodosomesSignal Transductionsrc-Family KinasesTransforming Growth Factor betaIntegrin beta3src-Family KinasesTransforming Growth Factor beta

Identifiers

PMID28767724
PMCPMC5540285
OpenAlexW2739541068

What OpenQuestion holds

Textmetadata
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.