Evidence map›Paper›PMID 25401739›Full record

ArticlePloS one2014

Wnt5a suppresses tumor formation and redirects tumor phenotype in MMTV-Wnt1 tumors.

Stephanie L Easter, Elizabeth H Mitchell, Sarah E Baxley, Renee Desmond, Andra R Frost, Rosa Serra

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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 1 citations in OpenAlex.

  1. Review
  2. 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

6 authors at 1 institution in 1 country.

Stephanie L EasterDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, 35294, United States of America.
Elizabeth H MitchellDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, 35294, United States of America.
Sarah E BaxleyDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, 35294, United States of America.
Renee DesmondDepartment of Medicine, Biostatistics and Bioinformatics Unit, Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL, 35294, United States of America.
Andra R FrostDepartment of Pathology, Division of Anatomic Pathology, University of Alabama at Birmingham, Birmingham, AL, 35294, United States of America.
Rosa SerraDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, 35294, United States of America.
University of Alabama at Birmingham · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Wnt5a and TGF-beta in mammary development and cancerR01CA126942 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SERRA, ROSA A. · 2009 to 2013
$1.5M
NCI NIH HHS P30 CA013148NCI NIH HHS P30 CA13148NCI NIH HHS R01 CA126942
6 · The paper itself

Abstract

Wnt5a is a non-canonical signaling Wnt that has been implicated in tumor suppression. We previously showed that loss of Wnt5a in MMTV-PyVmT tumors resulted in a switch in tumor phenotype resulting in tumors with increased basal phenotype and high Wnt/β-catenin signaling. The object of this study was to test the hypothesis that Wnt5a can act to inhibit tumors formed by activation of Wnt/β-catenin signaling. To this end, we characterized tumor and non-tumor mammary tissue from MMTV-Wnt1 and double transgenic MMTV-Wnt1;MMTV-Wnt5a mice. Wnt5a containing mice demonstrated fewer tumors with increased latency when compared to MMTV-Wnt1 controls. Expression of markers for basal-like tumors was down-regulated in the tumors that formed in the presence of Wnt5a indicating a phenotypic switch. Reduced canonical Wnt signaling was detected in double transgenic tumors as a decrease in active β-catenin protein and a decrease in Axin2 mRNA transcript levels. In non-tumor tissues, over-expression of Wnt5a in MMTV-Wnt1 mammary glands resulted in attenuation of phenotypes normally observed in MMTV-Wnt1 glands including hyperbranching and increased progenitor and basal cell populations. Even though Wnt5a could antagonize Wnt/β-catenin signaling in primary mammary epithelial cells in culture, reduced Wnt/β-catenin signaling was not detected in non-tumor MMTV-Wnt1;Wnt5a tissue in vivo. The data demonstrate that Wnt5a suppresses tumor formation and promotes a phenotypic shift in MMTV-Wnt1 tumors.

Indexed as

Animalsbeta CateninBlotting, WesternCells, CulturedEpithelial CellsFemaleFluorescent Antibody TechniqueImmunoenzyme TechniquesMaleMammary Glands, AnimalMammary Neoplasms, ExperimentalMammary Tumor Virus, MouseMiceMice, Inbred C57BLMice, TransgenicPhenotypebeta CateninRNA, MessengerWnt1 ProteinWnt1 protein, mouseWnt-5a ProteinWnt5a protein, mouseWnt Proteins

Identifiers

PMID25401739
PMCPMC4234660
OpenAlexW1994506276

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.