Evidence map›Paper›PMID 24981109›Full record

ReviewEndocrine-related cancer2014

Vangl1 and Vangl2: planar cell polarity components with a developing role in cancer.

Jason Hatakeyama, Jessica H Wald, Ignat Printsev, Hsin-Yi Henry Ho, Kermit L Carraway

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrine-related cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
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  15. Stearoylation cycle regulates the cell surface distribution of the PCP protein Vangl2.Proceedings of the National Academy of Sciences of the United States of America · 2024
    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

5 authors at 1 institution in 1 country.

Jason HatakeyamaDepartment of Biochemistry and Molecular MedicineUC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Research Building III, Room 1100B, 4645 2nd Avenue, Sacramento, California 95817, USADepartment of Cell Biology and Human AnatomyUC Davis School of Medicine, Davis, California 95616, USA.
Jessica H WaldDepartment of Biochemistry and Molecular MedicineUC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Research Building III, Room 1100B, 4645 2nd Avenue, Sacramento, California 95817, USADepartment of Cell Biology and Human AnatomyUC Davis School of Medicine, Davis, California 95616, USA.
Ignat PrintsevDepartment of Biochemistry and Molecular MedicineUC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Research Building III, Room 1100B, 4645 2nd Avenue, Sacramento, California 95817, USADepartment of Cell Biology and Human AnatomyUC Davis School of Medicine, Davis, California 95616, USA.
Hsin-Yi Henry HoDepartment of Biochemistry and Molecular MedicineUC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Research Building III, Room 1100B, 4645 2nd Avenue, Sacramento, California 95817, USADepartment of Cell Biology and Human AnatomyUC Davis School of Medicine, Davis, California 95616, USA.
Kermit L CarrawayDepartment of Biochemistry and Molecular MedicineUC Davis School of Medicine, UC Davis Comprehensive Cancer Center, Research Building III, Room 1100B, 4645 2nd Avenue, Sacramento, California 95817, USADepartment of Cell Biology and Human AnatomyUC Davis School of Medicine, Davis, California 95616, USA klcarraway@ucdavis.edu.
University of California, Davis · US

Funding

NRDP1 PROTEIN DEGRADATION PATHWAY IN MAMMARY TUMOR PROGRESSIONR01CA123541 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2006 to 2016
$2.5M
Muc4 Involvement in Mammary Tumor ProgressionR01CA166412 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2013 to 2017
$1.5M
Novel method of identifying circulating mammary tumor cellsR21CA178681 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARRAWAY, KERMIT L · 2013 to 2014
$362k
Negative regulation by proteasomal degradation of receptor tyrosine kinase ErbB3F31CA165546 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI PRINTSEV, IGNAT · 2012 to 2015
$143k
The role of the mucin Muc4 signaling in breast cancer formation and progressionF31CA165758 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HATAKEYAMA, JASON · 2012 to 2013
$70k
NCI NIH HHS CA123541NCI NIH HHS CA165546NCI NIH HHS CA165758NCI NIH HHS CA166412NCI NIH HHS CA178681NCI NIH HHS F31 CA165546NCI NIH HHS F31 CA165758NCI NIH HHS R01 CA123541NCI NIH HHS R01 CA166412NCI NIH HHS R21 CA178681
6 · The paper itself

Abstract

Cancers commonly reactivate embryonic developmental pathways to promote the aggressive behavior of their cells, resulting in metastasis and poor patient outcome. While developmental pathways such as canonical Wnt signaling and epithelial-to-mesenchymal transition have received much attention, our understanding of the role of the planar cell polarity (PCP) pathway in tumor progression remains rudimentary. Protein components of PCP, including a subset that overlaps with the canonical Wnt pathway, partition in polarized epithelial cells along the planar axis and are required for the establishment and maintenance of lateral epithelial polarity. Significant insight into PCP regulation of developmental and cellular processes has come from analysis of the functions of the core PCP scaffolding proteins Vangl1 and Vangl2. In particular, studies on zebrafish and with Looptail (Lp) mice, which harbor point mutations in Vangl2 that alter its trafficking and localization, point to roles for the PCP pathway in maintaining cell polarization along both the apical-basal and planar axes as well as in collective cell motility and invasiveness. Recent findings have suggested that the Vangls can promote similar processes in tumor cells. Initial data-mining efforts suggest that VANGL1 and VANGL2 are dysregulated in human cancers, and estrogen receptor (ER)-positive breast cancer patients whose tumors exhibit elevated VANGL1 expression suffer from shortened overall survival. Overall, evidence is beginning to accumulate that the heightened cellular motility and invasiveness associated with PCP reactivation may contribute to the malignancy of some cancer subtypes.

Indexed as

Cell PolarityAnimalsCarrier ProteinsEpithelial CellsHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeoplasmsCarrier ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsVANGL1 protein, humanVANGL2 protein, humanbreast cancercell migrationdevelopmental pathwaysinvasivenessplanar cell polaritypolarityVangl1Vangl2

Identifiers

PMID24981109
PMCPMC4332879
OpenAlexW2137518600

What OpenQuestion holds

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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.