Evidence map›Paper›PMID 26034982›Full record

ArticlePloS one2015

The Forkhead Transcription Factor FOXP2 Is Required for Regulation of p21WAF1/CIP1 in 143B Osteosarcoma Cell Growth Arrest.

Duncan M Gascoyne, Hayley Spearman, Linden Lyne, Rathi Puliyadi, Marta Perez-Alcantara, Les Coulton, Simon E Fisher, Peter I Croucher, Alison H Banham

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Tubular FoxP2 and Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025
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  6. Observational
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  10. Downregulation of miR-222-3p Reverses Doxorubicin-Resistance in LoVo Cells Through Upregulating Forkhead Box Protein P2 (FOXP2) Protein.Medical science monitor : international medical journal of experimental and clinical research · 2019
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  13. Review
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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

9 authors at 5 institutions in 3 countries.

Duncan M GascoyneNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, Oxford University, Oxford, OX3 9DU United Kingdom.
Hayley SpearmanNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, Oxford University, Oxford, OX3 9DU United Kingdom.
Linden LyneNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, Oxford University, Oxford, OX3 9DU United Kingdom.
Rathi PuliyadiWellcome Trust Centre for Human Genetics, Oxford, OX3 7BN United Kingdom.
Marta Perez-AlcantaraNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, Oxford University, Oxford, OX3 9DU United Kingdom.
Les CoultonAcademic Unit of Bone Biology, Dept of Human Metabolism, University of Sheffield, Sheffield, S10 2RX United Kingdom.
Simon E FisherLanguage and Genetics Department, Max Planck Institute for Psycholinguistics, and Donders Institute for Brain, Cognition and Behaviour, Nijmegen, The Netherlands.
Peter I CroucherGarvan Institute of Medical Research, Sydney, Australia.
Alison H BanhamNuffield Division of Clinical Laboratory Sciences, Radcliffe Department of Medicine, Oxford University, Oxford, OX3 9DU United Kingdom.
University of Oxford · GBCentre for Human Genetics · GBGarvan Institute of Medical Research · AUMax Planck Institute for Psycholinguistics · NLUniversity of Sheffield · GB

Funding

Wellcome TrustWellcome Trust 075491Wellcome Trust 080971
6 · The paper itself

Abstract

Mutations of the forkhead transcription factor FOXP2 gene have been implicated in inherited speech-and-language disorders, and specific Foxp2 expression patterns in neuronal populations and neuronal phenotypes arising from Foxp2 disruption have been described. However, molecular functions of FOXP2 are not completely understood. Here we report a requirement for FOXP2 in growth arrest of the osteosarcoma cell line 143B. We observed endogenous expression of this transcription factor both transiently in normally developing murine osteoblasts and constitutively in human SAOS-2 osteosarcoma cells blocked in early osteoblast development. Critically, we demonstrate that in 143B osteosarcoma cells with minimal endogenous expression, FOXP2 induced by growth arrest is required for up-regulation of p21WAF1/CIP1. Upon growth factor withdrawal, FOXP2 induction occurs rapidly and precedes p21WAF1/CIP1 activation. Additionally, FOXP2 expression could be induced by MAPK pathway inhibition in growth-arrested 143B cells, but not in traditional cell line models of osteoblast differentiation (MG-63, C2C12, MC3T3-E1). Our data are consistent with a model in which transient upregulation of Foxp2 in pre-osteoblast mesenchymal cells regulates a p21-dependent growth arrest checkpoint, which may have implications for normal mesenchymal and osteosarcoma biology.

Indexed as

ApoptosisGene Expression Regulation, NeoplasticAnimalsBlotting, WesternBone NeoplasmsCell CycleCell ProliferationCells, CulturedChromatin ImmunoprecipitationCyclin-Dependent Kinase Inhibitor p21Forkhead Transcription FactorsHumansImmunoenzyme TechniquesMaleMiceMice, Inbred C57BLCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21Forkhead Transcription FactorsFOXP2 protein, humanRNA, Messenger

Identifiers

PMID26034982
PMCPMC4452790
OpenAlexW1962911110

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.