Evidence map›Paper›PMID 25261235›Full record

ReviewCancer research2014

DEAR1, a novel tumor suppressor that regulates cell polarity and epithelial plasticity.

Nanyue Chen, Seetharaman Balasenthil, Jacquelyn Reuther, Ann McNeill Killary

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 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
1.1field-weighted citation impact, top 24% 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, 28 citations in OpenAlex.

  1. Article
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  16. Downregulation of TRIM21 contributes to hepatocellular carcinoma carcinogenesis and indicates poor prognosis of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

4 authors at 1 institution in 1 country.

Nanyue ChenDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Seetharaman BalasenthilDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Jacquelyn ReutherDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Program in Human and Molecular Genetics, University of Texas Graduate School of Biomedical Sciences, Houston, Texas.
Ann McNeill KillaryDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas. Program in Human and Molecular Genetics, University of Texas Graduate School of Biomedical Sciences, Houston, Texas. akillary@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Biomarkers for the Early Detection of Pancreatic CancerU01CA111302 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KILLARY, ANN M, SEN, SUBRATA · 2004 to 2015
$6.6M
NCI NIH HHS U01 CA111302
6 · The paper itself

Abstract

Elucidation of the regulatory controls on epithelial plasticity is pivotal not only to better understand the nature of metastasis but also for the design of targeted therapies to prevent the earliest steps in migration and invasion from the primary tumor. This review will highlight the role of the novel TRIM protein DEAR1 (annotated as TRIM62) in the regulation of apical-basal polarity and acinar morphogenesis as well as its function as a chromosome 1p35 tumor suppressor and negative regulator of TGFβ-driven epithelial-mesenchymal transition (EMT). DEAR1 binds to and promotes the ubiquitination of SMAD3, the major effector of TGFβ-mediated EMT, as well as downregulates SMAD3 targets SNAIL1/2, master transcriptional regulators of EMT. Cumulative results suggest a novel paradigm for DEAR1 in the regulation of the breast tumor microenvironment, polarity, and EMT. Because DEAR1 undergoes loss-of-function mutations, homozygous deletion, as well as copy-number losses in multiple epithelial cancers, including breast cancer, DEAR1 has clinical use as a predictive and prognostic biomarker as well as for stratifying breast cancers and potentially other epithelial tumor types for targeted therapies aimed at the pathways regulated by DEAR1.

Indexed as

Cell PolarityAnimalsBreast NeoplasmsEpithelial-Mesenchymal TransitionEpitheliumFemaleHumansNeoplasms, Glandular and EpithelialSignal TransductionTransforming Growth Factor betaTripartite Motif ProteinsTumor Suppressor ProteinsUbiquitinationUbiquitin-Protein LigasesTransforming Growth Factor betaTRIM62 protein, humanTripartite Motif ProteinsTumor Suppressor ProteinsUbiquitin-Protein Ligases

Identifiers

PMID25261235
PMCPMC4214267
OpenAlexW2060203699

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.