Evidence map›Paper›PMID 25122124›Full record

ArticlePloS one2014

Snail promotes epithelial mesenchymal transition in breast cancer cells in part via activation of nuclear ERK2.

Bethany N Smith, Liza J Burton, Veronica Henderson, Diandra D Randle, Derrick J Morton, Basil A Smith, Latonia Taliaferro-Smith, Peri Nagappan, Clayton Yates, Majd Zayzafoon and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 124 citations in OpenAlex.

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8 more citing papers are in PubMed but not listed here.

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 6 institutions in 1 country.

Bethany N SmithCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Liza J BurtonCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Veronica HendersonCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Diandra D RandleCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Derrick J MortonCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Basil A SmithCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Latonia Taliaferro-SmithThe Department of Hematology and Medical Oncology and Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Peri NagappanCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Clayton YatesDepartment of Biology, Tuskegee University, Tuskegee, Alabama, United States of America.
Majd ZayzafoonThe Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
Leland W K ChungThe Uro-Oncology Research Program, Department of Medicine, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Valerie A Odero-MarahCenter for Cancer Research and Therapeutic Development and Department of Biological Sciences, Clark Atlanta University, Atlanta, Georgia, United States of America.
Clark Atlanta University · USCenter for Cancer Research · USCedars-Sinai Medical Center · USTuskegee University · USUniversity of Alabama at Birmingham · USWinship Cancer Institute

Funding

TRAINING AND CAREER DEVELOPMENTU54CA118948 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Timiya S Nolan · 2005 to 2026
$26.6M
Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI ZAYZAFOON, MAJD · 2003 to 2019
$24.0M
Research Education CoreU54CA118623 · NCI · TUSKEGEE UNIVERSITY · PI STEPHEN O SODEKE · 2005 to 2026
$20.2M
THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI CHAUDHARY, JAIDEEP · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
INFRASTRUCTURE IIG12MD007585 · NIMHD · TUSKEGEE UNIVERSITY · PI YATES, CLAYTON · 2012 to 2016
$4.6M
NCI NIH HHS P01 CA098912NCI NIH HHS U54 CA118623NCI NIH HHS U54 CA118948NCRR NIH HHS G12 RR003062NCRR NIH HHS G12RR003062-22NIMHD NIH HHS G12 MD007585NIMHD NIH HHS G12 MD007590NIMHD NIH HHS P20 MD002285NIMHD NIH HHS P20MD002285-01
6 · The paper itself

Abstract

Snail transcription factor is up-regulated in several cancers and associated with increased tumor migration and invasion via induction of epithelial-to-mesenchymal transition (EMT). MAPK (ERK1/2) signaling regulates cellular processes including cell motility, adhesion, and invasion. We investigated the regulation of ERK1/2 by Snail in breast cancer cells. ERK1/2 activity (p-ERK) was higher in breast cancer patient tissue as compared to normal tissue. Snail and p-ERK were increased in several breast cancer cell lines as compared to normal mammary epithelial cells. Snail knockdown in MDA-MB-231 and T47-D breast cancer cells decreased or re-localized p-ERK from the nuclear compartment to the cytoplasm. Snail overexpression in MCF-7 breast cancer cells induced EMT, increased cell migration, decreased cell adhesion and also increased tumorigenicity. Snail induced nuclear translocation of p-ERK, and the activation of its subcellular downstream effector, Elk-1. Inhibiting MAPK activity with UO126 or knockdown of ERK2 isoform with siRNA in MCF-7 Snail cells reverted EMT induced by Snail as shown by decreased Snail and vimentin expression, decreased cell migration and increased cell adhesion. Overall, our data suggest that ERK2 isoform activation by Snail in aggressive breast cancer cells leads to EMT associated with increased cell migration and decreased cell adhesion. This regulation is enhanced by positive feedback regulation of Snail by ERK2. Therefore, therapeutic targeting of ERK2 isoform may be beneficial for breast cancer.

Indexed as

AnimalsBreast NeoplasmsCell NucleusEpithelial-Mesenchymal TransitionFemaleHumansMCF-7 CellsMiceMice, NudeMitogen-Activated Protein Kinase 1Proteasome Endopeptidase ComplexProtein TransportSnail Family Transcription FactorsTranscription FactorsMAPK1 protein, humanMitogen-Activated Protein Kinase 1Proteasome Endopeptidase ComplexSnail Family Transcription FactorsTranscription Factors

Identifiers

PMID25122124
PMCPMC4133359
OpenAlexW2072642940

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.