Evidence map›Paper›PMID 25371204›Full record

ArticleThe Journal of biological chemistry2014

The anti-proliferative function of the TGF-β1 signaling pathway involves the repression of the oncogenic TBX2 by its homologue TBX3.

Jarod Li, Deeya Ballim, Mercedes Rodriguez, Rutao Cui, Colin R Goding, Huajian Teng, Sharon Prince

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

  1. Genes & diseases · 2026
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  9. Arterial dissections: Common features and new perspectives.Frontiers in cardiovascular medicine · 2022
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  17. Expression level ofOncology letters · 2018
    Article
  18. Article
  19. Expression, function, and regulation of the embryonic transcription factor TBX1 in parathyroid tumors.Laboratory investigation; a journal of technical methods and pathology · 2017
    Article
  20. 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

7 authors at 3 institutions in 3 countries.

Jarod LiFrom the Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, 7925, Cape Town, South Africa.
Deeya BallimFrom the Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, 7925, Cape Town, South Africa.
Mercedes RodriguezLudwig Institute for Cancer Research, Oxford University, Headington, Oxford OX3 7DQ, United Kingdom, and.
Rutao CuiDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, Massachusetts 02118.
Colin R GodingLudwig Institute for Cancer Research, Oxford University, Headington, Oxford OX3 7DQ, United Kingdom, and.
Huajian TengFrom the Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, 7925, Cape Town, South Africa.
Sharon PrinceFrom the Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, 7925, Cape Town, South Africa, sharon.prince@uct.ac.za.
University of Cape Town · ZALudwig Cancer Research · GBBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A growing body of work has shown that the highly homologous T-box transcription factors TBX2 and TBX3 play critical but distinct roles in embryonic development and cancer progression. For example, TBX2 and TBX3 are up-regulated in several cancers and recent evidence suggests that whereas TBX2 functions as a pro-proliferative factor, TBX3 inhibits cell proliferation but promotes cancer cell migration and invasion. While the molecular mechanisms regulating these functions of TBX2 and TBX3 are poorly understood we recently reported that the TGF-β1 signaling pathway up-regulates TBX3 expression to mediate, in part, its well described anti-proliferative and pro-migratory roles. The TBX3 targets responsible for these functions were however not identified. Here we reveal for the first time that the TGF-β1 signaling pathway represses TBX2 transcriptionally and we provide a detailed mechanism to show that this is mediated by TBX3. Furthermore, we implicate the down-regulation of TBX2 in the anti-proliferative function of the TGF-β1-TBX3 axis. These findings have important implications for our understanding of the regulation of TBX2 and TBX3 and shed light on the mechanisms involved in the anti-proliferative and pro-migratory roles of TGF-β1.

Indexed as

AnimalsBinding SitesBlotting, WesternCell LineCell Line, TumorCell ProliferationDown-RegulationGene ExpressionHumansMutationOncogene ProteinsPromoter Regions, GeneticProtein BindingReverse Transcriptase Polymerase Chain ReactionRNA InterferenceSignal TransductionOncogene ProteinsT-Box Domain Protein 2T-Box Domain ProteinsTBX3 protein, humanTransforming Growth Factor beta1Cell CycleCell ProliferationGene Expressionp21TBX2TBX3Transcription FactorTransforming Growth Factor β (TGF-β)

Identifiers

PMID25371204
PMCPMC4271245
OpenAlexW1990998396

What OpenQuestion holds

Textmetadata
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.