Evidence map›Paper›PMID 22541669›Full record

ArticleSkeletal muscle2012

miR-206 integrates multiple components of differentiation pathways to control the transition from growth to differentiation in rhabdomyosarcoma cells.

Kyle L Macquarrie, Zizhen Yao, Janet M Young, Yi Cao, Stephen J Tapscott

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-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

29 citing papers in PubMed, 43 citations in OpenAlex.

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  18. MiR-206, a key modulator of skeletal muscle development and disease.International journal of biological sciences · 2015
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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

5 authors at 2 institutions in 1 country.

Kyle L MacquarrieHuman Biology Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, C3-168, Seattle, WA, 98109, USA. stapscot@fhcrc.org.
Zizhen Yao
Janet M Young
Yi Cao
Stephen J Tapscott
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

LINEAGE DETERMINATION IN MUSCLER01AR045113 · NIAMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TAPSCOTT, STEPHEN J · 1998 to 2017
$6.8M
INTERDISCIPLINARY TRAINING IN DEVELOPMENTAL BIOLOGYT32HD007183 · NICHD · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2015
$5.7M
NIAMS NIH HHS R01 AR045113NICHD NIH HHS T32 HD007183
6 · The paper itself

Abstract

backgroundSimilar to replicating myoblasts, many rhabdomyosarcoma cells express the myogenic determination gene MyoD. In contrast to myoblasts, rhabdomyosarcoma cells do not make the transition from a regulative growth phase to terminal differentiation. Previously we demonstrated that the forced expression of MyoD with its E-protein dimerization partner was sufficient to induce differentiation and suppress multiple growth-promoting genes, suggesting that the dimer was targeting a switch that regulated the transition from growth to differentiation. Our data also suggested that a balance between various inhibitory transcription factors and MyoD activity kept rhabdomyosarcomas trapped in a proliferative state.

methodsPotential myogenic co-factors were tested for their ability to drive differentiation in rhabdomyosarcoma cell culture models, and their relation to MyoD activity determined through molecular biological experiments.

resultsModulation of the transcription factors RUNX1 and ZNF238 can induce differentiation in rhabdomyosarcoma cells and their activity is integrated, at least in part, through the activation of miR-206, which acts as a genetic switch to transition the cell from a proliferative growth phase to differentiation. The inhibitory transcription factor MSC also plays a role in controlling miR-206, appearing to function by occluding a binding site for MyoD in the miR-206 promoter.

conclusionsThese findings support a network model composed of coupled regulatory circuits with miR-206 functioning as a switch regulating the transition from one stable state (growth) to another (differentiation).

Identifiers

PMID22541669
PMCPMC3417070
OpenAlexW2130528799

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.