Evidence map›Paper›PMID 24107628›Full record

ArticleCell cycle (Georgetown, Tex.)2013

Cyclin D1 is a major target of miR-206 in cell differentiation and transformation.

Alessandra Alteri, Francesca De Vito, Graziella Messina, Monica Pompili, Attilio Calconi, Paolo Visca, Marcella Mottolese, Carlo Presutti, Milena Grossi

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  5. Review
  6. miR-152 Regulates Bovine Myoblast Proliferation by Targeting KLF6.Animals : an open access journal from MDPI · 2021
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  9. Review
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  13. The oncomir face of microRNA-206: A permanent miR-206 transfection study.Experimental biology and medicine (Maywood, N.J.) · 2018
    Article
  14. Article
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  16. Article
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  18. Article
  19. miR-206-3p Inhibits 3T3-L1 Cell Adipogenesis via the c-Met/PI3K/Akt Pathway.International journal of molecular sciences · 2017
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Alessandra AlteriDipartimento di Biologia e Biotecnologie "C. Darwin"; Sapienza-Università di Roma; Roma, Italy.
Francesca De VitoDipartimento di Biologia e Biotecnologie "C. Darwin"; Sapienza-Università di Roma; Roma, Italy.
Graziella MessinaDipartimento di Bioscienze; Università di Milano; Milano, Italy.
Monica PompiliDipartimento di Biologia e Biotecnologie "C. Darwin"; Sapienza-Università di Roma; Roma, Italy.
Attilio CalconiDipartimento di Biologia e Biotecnologie "C. Darwin"; Sapienza-Università di Roma; Roma, Italy.
Paolo ViscaAnatomia Patologica; Istituto Nazionale Tumori Regina Elena; Roma, Italy.
Marcella MottoleseAnatomia Patologica; Istituto Nazionale Tumori Regina Elena; Roma, Italy.
Carlo PresuttiDipartimento di Biologia e Biotecnologie "C. Darwin"; Sapienza-Università di Roma; Roma, Italy.
Milena GrossiDipartimento di Biologia e Biotecnologie "C. Darwin"; Sapienza-Università di Roma; Roma, Italy.
Sapienza University of Rome · ITAnthrologica · GBCentro di Riferimento Oncologico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

miR-206, a member of the so-called myomiR family, is largely acknowledged as a specific, positive regulator of skeletal muscle differentiation. A growing body of evidence also suggests a tumor suppressor function for miR-206, as it is frequently downregulated in various types of cancers. In this study, we show that miR-206 directly targets cyclin D1 and contributes to the regulation of CCND1 gene expression in both myogenic and non-muscle, transformed cells. We demonstrate that miR-206, either exogenous or endogenous, reduces cyclin D1 levels and proliferation rate in C2C12 cells without promoting differentiation, and that miR-206 knockdown in terminally differentiated C2C12 cells leads to cyclin D1 accumulation in myotubes, indicating that miR-206 might be involved in the maintenance of the post-mitotic state. Targeting of cyclin D1 might also account, at least in part, for the tumor-suppressor activity suggested for miR-206 in previous studies. Accordingly, the analysis of neoplastic and matched normal lung tissues reveals that miR-206 downregulation in lung tumors correlates, in most cases, with higher cyclin D1 levels. Moreover, gain-of-function experiments with cancer-derived cell lines and with in vitro transformed cells indicate that miR-206-mediated cyclin D1 repression is directly coupled to growth inhibition. Altogether, our data highlight a novel activity for miR-206 in skeletal muscle differentiation and identify cyclin D1 as a major target that further strengthens the tumor suppressor function proposed for miR-206.

Indexed as

AdenocarcinomaCell DifferentiationCell Line, TransformedCell Line, TumorCell Transformation, NeoplasticCyclin D1HumansLung NeoplasmsMicroRNAsMuscle, SkeletalOrgan SpecificityCyclin D1MicroRNAsMIRN206 microRNA, humancell proliferationcell transformationcyclin D1miR-206myogenic differentiation

Identifiers

PMID24107628
PMCPMC3905070
OpenAlexW2013217382

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.