Evidence map›Paper›PMID 22808202›Full record

ArticlePloS one2012

Rac1 activation driven by 14-3-3ζ dimerization promotes prostate cancer cell-matrix interactions, motility and transendothelial migration.

Anna Goc, Maha Abdalla, Ahmad Al-Azayzih, Payaningal R Somanath

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. hsa-MicroRNA-28-5p Inhibits Diffuse Large B-Cell Lymphoma Cell Proliferation by Downregulating 14-3-3Evidence-based complementary and alternative medicine : eCAM · 2022
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  12. Interaction between Rho GTPases and 14-3-3 Proteins.International journal of molecular sciences · 2017
    Review
  13. Article
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  20. A cancer-related protein 14-3-3ζ is a potential tumor-associated antigen in immunodiagnosis of hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    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

4 authors at 3 institutions in 1 country.

Anna GocClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, Georgia, United States of America.
Maha Abdalla
Ahmad Al-Azayzih
Payaningal R Somanath
University of Georgia · USAugusta University · USAugusta University Health · US

Funding

Protein kinase B (Akt)-mediated pathway regulating endothelial-barrier functionR01HL103952 · NHLBI · UNIVERSITY OF GEORGIA · PI SHENOY, SOMANATH P RAMMOHAN · 2011 to 2015
$1.5M
NHLBI NIH HHS (R01HL103952NHLBI NIH HHS R01 HL103952
6 · The paper itself

Abstract

14-3-3 proteins are ubiquitously expressed dimeric adaptor proteins that have emerged as key mediators of many cell signaling pathways in multiple cell types. Its effects are mainly mediated by binding to selective phosphoserine/threonine proteins. The importance of 14-3-3 proteins in cancer have only started to become apparent and its exact role in cancer progression as well as the mechanisms by which 14-3-3 proteins mediate cancer cell function remain unknown. While protein 14-3-3σ is widely accepted as a tumor suppressor, 14-3-3ζ, β and γ isoforms have been shown to have tumor promoting effects. Despite the importance of 14-3-3 family in mediating various cell processes, the exact role and mechanism of 14-3-3ζ remain unexplored. In the current study, we investigated the role of protein 14-3-3ζ in prostate cancer cell motility and transendothelial migration using biochemical, molecular biology and electric cell-substrate impedance sensing approaches as well as cell based functional assays. Our study indicated that expression with wild-type protein 14-3-3ζ significantly enhanced Rac activity in PC3 cells. In contrast, expression of dimer-resistant mutant of protein 14-3-3ζ (DM-14-3-3) inhibited Rac activity and associated phosphorylation of p21 activated kinase-1 and 2. Expression with wild-type 14-3-3ζ or constitutively active Rac1 enhanced extracellular matrix recognition, lamellipodia formation, cell migration and trans-endothelial migration by PC3 cells. In contrast, expression with DM 14-3-3ζ or DN-Rac1 in PC3 cells significantly inhibited these cell functions. Our results demonstrate for the first time that 14-3-3ζ enhances prostate cancer cell-matrix interactions, motility and transendothelial migration in vitro via activation of Rac1-GTPase and is an important target for therapeutic interventions for prostate cancer.

Indexed as

Protein MultimerizationTransendothelial and Transepithelial Migration14-3-3 ProteinsAnimalsCell Line, TumorCell Transformation, NeoplasticEnzyme ActivationEpidermal Growth FactorExtracellular MatrixHumansMaleMicep21-Activated KinasesProstatic NeoplasmsProtein BindingPseudopodia14-3-3 ProteinsEpidermal Growth Factorp21-Activated Kinasesrac1 GTP-Binding ProteinRAC1 protein, humanYWHAZ protein, human

Identifiers

PMID22808202
PMCPMC3396618
OpenAlexW2060797107

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.