Evidence map›Paper›PMID 24553076›Full record

ArticleOncotarget2014

P-cadherin signals through the laminin receptor α6β4 integrin to induce stem cell and invasive properties in basal-like breast cancer cells.

André Filipe Vieira, Ana Sofia Ribeiro, Maria Rita Dionísio, Bárbara Sousa, Ana Rita Nobre, André Albergaria, Angélica Santiago-Gómez, Nuno Mendes, Renê Gerhard, Fernando Schmitt and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Cancers · 2025
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  13. Cancer-Cell-Derived IgG and Its Potential Role in Tumor Development.International journal of molecular sciences · 2021
    Review
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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

12 authors at 3 institutions in 2 countries.

André Filipe VieiraIPATIMUP - Institute of Molecular Pathology and Immunology of the University of Porto, Porto, Portugal.
Ana Sofia Ribeiro
Maria Rita Dionísio
Bárbara Sousa
Ana Rita Nobre
André Albergaria
Angélica Santiago-Gómez
Nuno Mendes
Renê Gerhard
Fernando Schmitt
Robert B Clarke
Joana Paredes
Universidade do Porto · PTUniversity of Manchester · GBInstituto Gulbenkian de Ciência · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P-cadherin is a classical cell-cell adhesion molecule that, in contrast to E-cadherin, has a positive role in breast cancer progression, being considered a poor prognostic factor in this disease. In previous reports, we have shown that this protein induces cancer stem cell and invasive properties to basal-like breast cancer cells. Here, we clarify the downstream signaling pathways that are triggered by P-cadherin to mediate these effects. We demonstrated that P-cadherin inhibition led to a significant decreased adhesion of cancer cells to the basement membrane substrate laminin, as well as to a major reduction in the expression of the laminin receptor α6β4 integrin. Remarkably, the expression of this heterodimer was required for the invasive capacity and increased mammosphere forming efficiency induced by P-cadherin expression. Moreover, we showed that P-cadherin transcriptionally up-regulates the α6 integrin subunit expression and directly interacts with the β4 integrin subunit. We still showed that P-cadherin downstream signaling, in response to laminin, involves the activation of focal adhesion (FAK), Src and AKT kinases. The association between the expression of P-cadherin, α6β4 heterodimer and the active FAK and Src phosphorylated forms was validated in vivo. Our data establish that there is a crosstalk between P-cadherin and the laminin receptor α6β4 integrin signaling pathway, which link has never been previously described. The activation of this heterodimer explains the stem cell and invasive properties induced by P-cadherin to breast cancer cells, pointing to a new molecular mechanism that may be targeted to counteract the effects induced by this adhesion molecule.

Indexed as

AnimalsBreast NeoplasmsCadherinsCell AdhesionCell Line, TumorFemaleHeterograftsHumansIntegrin alpha6beta4MCF-7 CellsMiceMice, NudeNeoplasm InvasivenessNeoplastic Stem CellsPhosphorylationSignal TransductionCadherinsIntegrin alpha6beta4

Identifiers

PMID24553076
PMCPMC3996674
OpenAlexW2120825444

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.