Evidence map›Paper›PMID 24950909›Full record

ArticleCancer research2014

TRIM29 suppresses TWIST1 and invasive breast cancer behavior.

Lingbao Ai, Wan-Ju Kim, Merve Alpay, Ming Tang, Carolina E Pardo, Shigetsugu Hatakeyama, W Stratford May, Michael P Kladde, Coy D Heldermon, Erin M Siegel and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

51 citing papers in PubMed, 88 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Lingbao AiDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida. lingbao@ufl.edu kdbrown1@ufl.edu.
Wan-Ju KimDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida.
Merve AlpayDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida.
Ming TangDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida.
Carolina E PardoDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida.
Shigetsugu HatakeyamaDepartment of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
W Stratford MayUF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida. Department of Medicine, University of Florida College of Medicine, Gainesville, Florida.
Michael P KladdeDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida.
Coy D HeldermonUF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida. Department of Medicine, University of Florida College of Medicine, Gainesville, Florida.
Erin M SiegelDivision of Population Sciences, Cancer Epidemiology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida. Department of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Kevin D BrownDepartment of Biochemistry and Molecular Biology, University of Florida College of Medicine, Gainesville, Florida. UF-Health Cancer Center, University of Florida College of Medicine, Gainesville, Florida. lingbao@ufl.edu kdbrown1@ufl.edu.
University of Florida Health · USHokkaido University · JPMoffitt Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Interplay of Epigenetic Mechanisms in Gene SilencingR01CA155390 · NCI · UNIVERSITY OF FLORIDA · PI KLADDE, MICHAEL PAUL · 2011 to 2015
$1.5M
Defining Novel Biomarkers for Cervical Cancer Etiology and Progression by QuantitR03CA143980 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI SIEGEL, ERIN · 2009 to 2010
$175k
NCI NIH HHS 1R03CA143980NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA155390NCI NIH HHS R03 CA143980
6 · The paper itself

Abstract

TRIM29 (ATDC) exhibits a contextual function in cancer, but seems to exert a tumor-suppressor role in breast cancer. Here, we show that TRIM29 is often silenced in primary breast tumors and cultured tumor cells as a result of aberrant gene hypermethylation. RNAi-mediated silencing of TRIM29 in breast tumor cells increased their motility, invasiveness, and proliferation in a manner associated with increased expression of mesenchymal markers (N-cadherin and vimentin), decreased expression of epithelial markers (E-cadherin and EpCAM), and increased expression and activity of the oncogenic transcription factor TWIST1, an important driver of the epithelial-mesenchymal transition (EMT). Functional investigations revealed an inverse relationship in the expression of TRIM29 and TWIST1, suggesting the existence of a negative regulatory feedback loop. In support of this relationship, we found that TWIST1 inhibited TRIM29 promoter activity through direct binding to a region containing a cluster of consensus E-box elements, arguing that TWIST1 transcriptionally represses TRIM29 expression. Analysis of a public breast cancer gene-expression database indicated that reduced TRIM29 expression was associated with reduced relapse-free survival, increased tumor size, grade, and metastatic characteristics. Taken together, our results suggest that TRIM29 acts as a tumor suppressor in breast cancer through its ability to inhibit TWIST1 and suppress EMT.

Indexed as

Antigens, NeoplasmBreast NeoplasmsCadherinsCell Adhesion MoleculesCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsDNA MethylationE-Box ElementsEpithelial Cell Adhesion MoleculeEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessAntigens, NeoplasmCadherinsCell Adhesion MoleculesDNA-Binding ProteinsEPCAM protein, humanEpithelial Cell Adhesion MoleculeNuclear ProteinsTranscription FactorsTRIM29 protein, humanTWIST1 protein, humanTwist-Related Protein 1Vimentin

Identifiers

PMID24950909
PMCPMC4329918
OpenAlexW2068274629

What OpenQuestion holds

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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.