Evidence map›Paper›PMID 34819350›Full record

ArticleGenes & development2021

TBX2 controls a proproliferative gene expression program in melanoma.

Sizhu Lu, Pakavarin Louphrasitthiphol, Nishit Goradia, Jean-Philippe Lambert, Johannes Schmidt, Jagat Chauhan, Milap G Rughani, Lionel Larue, Matthias Wilmanns, Colin R Goding

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  7. Review
  8. Revisiting the Potency of Tbx2 Expression in Transforming Outer Hair Cells into Inner Hair Cells at Multiple Ages In Vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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

10 authors at 6 institutions in 5 countries.

Sizhu LuLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Pakavarin LouphrasitthipholLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Nishit GoradiaEuropean Molecular Biology Laboratory, Hamburg Unit, 22607 Hamburg, Germany.
Jean-Philippe LambertLunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada.
Johannes SchmidtLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Jagat ChauhanLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Milap G RughaniLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Lionel LarueInstitut Curie, PSL Research University, U1021, Institut National de la Santé et de la Recherche Médicale, Normal and Pathological Development of Melanocytes, 91405 Orsay Cedex, France.
Matthias WilmannsEuropean Molecular Biology Laboratory, Hamburg Unit, 22607 Hamburg, Germany.
Colin R GodingLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Headington, Oxford OX3 7DQ, United Kingdom.
Ludwig Cancer Research · GBUniversity of Oxford · GBEuropean Molecular Biology Laboratory · DELunenfeld-Tanenbaum Research Institute · CAUniversité Paris-Sud · FRUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Senescence shapes embryonic development, plays a key role in aging, and is a critical barrier to cancer initiation, yet how senescence is regulated remains incompletely understood. TBX2 is an antisenescence T-box family transcription repressor implicated in embryonic development and cancer. However, the repertoire of TBX2 target genes, its cooperating partners, and how TBX2 promotes proliferation and senescence bypass are poorly understood. Here, using melanoma as a model, we show that TBX2 lies downstream from PI3K signaling and that TBX2 binds and is required for expression of E2F1, a key antisenescence cell cycle regulator. Remarkably, TBX2 binding in vivo is associated with CACGTG E-boxes, present in genes down-regulated by TBX2 depletion, more frequently than the consensus T-element DNA binding motif that is restricted to Tbx2 repressed genes. TBX2 is revealed to interact with a wide range of transcription factors and cofactors, including key components of the BCOR/PRC1.1 complex that are recruited by TBX2 to the

Indexed as

MelanomaT-Box Domain ProteinsGene ExpressionHumansPhosphatidylinositol 3-KinasesTranscription FactorsPhosphatidylinositol 3-KinasesT-Box Domain ProteinsTranscription Factorscell cycleDNA bindingDNA binding specificityproliferationsenescenceTBX2

Identifiers

PMID34819350
PMCPMC8653791
OpenAlexW3208830524

What OpenQuestion holds

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LicenceCC BY
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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.