Evidence map›Paper›PMID 24771004›Full record

ArticleHormones & cancer2014

Membrane-initiated estradiol signaling of epithelial-mesenchymal transition-associated mechanisms through regulation of tight junctions in human breast cancer cells.

Javier E Jiménez-Salazar, Pedro Posadas-Rodríguez, Roberto C Lazzarini-Lechuga, Armando Luna-López, Alejandro Zentella-Dehesa, Luis E Gómez-Quiroz, Mina Königsberg, Guadalupe Domínguez-Gómez, Pablo Damián-Matsumura

Open access · bronzeAbstract read
In one paragraph

Article in Hormones & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  6. Review
  7. Mechanical stress shapes the cancer cell response to neddylation inhibition.Journal of experimental & clinical cancer research : CR · 2022
    Article
  8. Review
  9. Article
  10. Expression of Tight Junction Proteins Is Altered in Bladder Cancer.Analytical cellular pathology (Amsterdam) · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. Immunophenotypic profile of tumor buds in breast cancer.Pathology, research and practice · 2018
    Article
  15. Review
  16. 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

9 authors at 2 institutions in 1 country.

Javier E Jiménez-SalazarDepartment of Biology of Reproduction, Universidad Autonoma Metropolitana (UAM), 09310, Mexico City, Mexico.
Pedro Posadas-Rodríguez
Roberto C Lazzarini-Lechuga
Armando Luna-López
Alejandro Zentella-Dehesa
Luis E Gómez-Quiroz
Mina Königsberg
Guadalupe Domínguez-Gómez
Pablo Damián-Matsumura
Universidad Autónoma Metropolitana · MXInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor cells utilize inappropriate epithelial-mesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We demonstrated that 1 nM E2 elicits c-Src activation after 15 min. The p-Src/ZO-1 complex led to ZO-1 and ZONAB disruption at the TJ and increased expression of HER2 mRNAs. These changes correlate with decreased expression of the epithelial markers occludin and CRB3 and increased synthesis of N-cadherin. This led to increased MCF-7 cell migration induced by E2, even in the presence of a cell proliferation inhibitor. Incubation with ICI 182,780 (Fulvestrant), an ER antagonist, precluded the effects of E2 on c-Src phosphorylation, p-Src/ZO-1 complex formation, ZO-1/ZONAB nuclear translocation, and migration of MCF-7 cells. Our findings suggest that E2 promotes TJ disruption during tumor progression and increases cell motility. We propose a novel pathway where estrogens promote EMT-associated mechanisms that possibly lead to metastasis.

Indexed as

Epithelial-Mesenchymal TransitionActive Transport, Cell NucleusBreast NeoplasmsCadherinsCell Line, TumorCell MovementCSK Tyrosine-Protein KinaseEstradiolFemaleHumansReceptors, EstrogenSignal Transductionsrc-Family KinasesTight JunctionsZonula Occludens-1 ProteinCadherinsCSK protein, humanCSK Tyrosine-Protein KinaseEstradiolReceptors, Estrogensrc-Family KinasesTJP1 protein, humanZonula Occludens-1 Protein

Identifiers

PMID24771004
PMCPMC10358110
OpenAlexW2166918352

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.