Evidence map›Paper›PMID 24491810›Full record

ArticleBiochimica et biophysica acta2014

MEKK2 regulates focal adhesion stability and motility in invasive breast cancer cells.

Ahmed A Mirza, Michael P Kahle, Magdalene Ameka, Edward M Campbell, Bruce D Cuevas

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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  6. Article
  7. Mucinous carcinoma with micropapillary features is morphologically, clinically and genetically distinct from pure mucinous carcinoma of breast.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  8. Article
  9. Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Oncogenic signaling of MEK5-ERK5.Cancer letters · 2017
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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

5 authors at 1 institution in 1 country.

Ahmed A MirzaDepartment of Molecular Pharmacology and Therapeutics, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA.
Michael P KahleDepartment of Molecular Pharmacology and Therapeutics, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA.
Magdalene AmekaDepartment of Molecular Pharmacology and Therapeutics, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA.
Edward M CampbellDepartment of Molecular Pharmacology and Therapeutics, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA.
Bruce D CuevasDepartment of Molecular Pharmacology and Therapeutics, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA. Electronic address: bcuevas@lumc.edu.
Loyola University Chicago · US

Funding

The role of MEKK1-dependent gene expression in tumor progressionK01CA120881 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CUEVAS, BRUCE D · 2007 to 2011
$711k
NCI NIH HHS CA120881NCI NIH HHS K01 CA120881
6 · The paper itself

Abstract

MEK Kinase 2 (MEKK2) is a serine/threonine kinase that functions as a MAPK kinase kinase (MAP3K) to regulate activation of Mitogen-activated Protein Kinases (MAPKs). We recently have demonstrated that ablation of MEKK2 expression in invasive breast tumor cells dramatically inhibits xenograft metastasis, but the mechanism by which MEKK2 influences metastasis-related tumor cell function is unknown. In this study, we investigate MEKK2 function and demonstrate that silencing MEKK2 expression in breast tumor cell significantly enhances cell spread area and focal adhesion stability while reducing cell migration. We show that cell attachment to the matrix proteins fibronectin or Matrigel induces MEKK2 activation and localization to focal adhesions. Further, we reveal that MEKK2 ablation enhances focal adhesion size and frequency, thereby linking MEKK2 function to focal adhesion stability. Finally, we show that MEKK2 knockdown inhibits fibronectin-induced Extracellular Signal-Regulated Kinase 5 (ERK5) signaling and Focal Adhesion Kinase (FAK) autophosphorylation. Taken together, our results strongly support a role for MEKK2 as a regulator of signaling that modulates breast tumor cell spread area and migration through control of focal adhesion stability.

Indexed as

Neoplasm InvasivenessBreast NeoplasmsCell Line, TumorFemaleFibronectinsFocal Adhesion Protein-Tyrosine KinasesFocal AdhesionsGene SilencingHumansMAP Kinase Kinase Kinase 2MAP Kinase Kinase KinasesPhosphorylationFibronectinsFocal Adhesion Protein-Tyrosine KinasesMAP3K2 protein, humanMAP Kinase Kinase Kinase 2MAP Kinase Kinase KinasesFibronectinFocal adhesionKinaseMEKK2

Identifiers

PMID24491810
PMCPMC3960922
OpenAlexW2060894178

What OpenQuestion holds

Textmetadata
LicenceTDM
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.