Evidence map›Paper›PMID 25111862›Full record

ArticleOncogenesis2014

Selective repression of the oncogene cyclin D1 by the tumor suppressor miR-206 in cancers.

S J Elliman, B V Howley, D S Mehta, H O Fearnhead, D M Kemp, L R Barkley

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Systemic Drug Effects in Vortioxetine-Induced Time-Series Datasets.International journal of molecular sciences · 2026
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  15. Circular RNAs are abundant and dynamically expressed during embryonic muscle development in chickens.DNA research : an international journal for rapid publication of reports on genes and genomes · 2018
    Article
  16. MiR-206 is down-regulated and suppresses cell proliferation by targeting FOXP1 in brain gliomas.International journal of clinical and experimental pathology · 2018
    Article
  17. Article
  18. [Role of miR-206/CDK4 in modulating the growth and chemotlerapy sensitivity of ovarian cancer cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017
    Article
  19. 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

6 authors at 3 institutions in 2 countries.

S J EllimanOrbsen Therapeutics Ltd, Galway, Ireland.
B V HowleyNational Centre for Biomedical Engineering Science, National University of Ireland Galway, Galway, Ireland.
D S MehtaBiogen Idec, Inc., Cambridge, MA, USA.
H O FearnheadPharmacology and Therapeutics, National University of Ireland Galway, Galway, Ireland.
D M KempEmerald Bio, Boston, MA, USA.
L R BarkleyNational Centre for Biomedical Engineering Science, National University of Ireland Galway, Galway, Ireland.
Ollscoil na Gaillimhe – University of Galway · IEBiogen (United States) · USOrbsen Therapeutics (Ireland) · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) are deregulated in cancer and have been shown to exhibit both oncogenic and tumor suppressive functions. Although the functional effects of several miRNAs have been elucidated, those of many remain to be discovered. In silico analysis identified microRNA-206 (miR-206) binding sites in the 3'-untranslated regions (3'-UTR) of both the mouse and human CCND1 gene. Cyclin D1 is a recognized oncogene involved in direct phosphorylation of the retinoblastoma (Rb) protein and promoting cell cycle transition from G1 to S. miR-206 specifically binds to the CCND1 3'-UTR and mediates reduction of both cyclin D1 protein and mRNA. Expression of miR-206 induced a G1 arrest and a decrease in cell proliferation in breast cancer cells. Ectopic expression of miRNA-resistant cyclin D1 was able to reverse the miR-206-induced decrease in cell proliferation. Therefore, we identified miR-206 as an activator of cell cycle arrest resulting in a decrease in cell proliferation that is dependent on the inhibition of cyclin D1. Interestingly, prostatic cancer (PCa) cells express low levels of miR-206 resulting in deregulated cyclin D1 expression compared with non-transformed primary prostatic epithelial cells (PrEC). Finally, we demonstrate that cyclin D1 is regulated by miR-206 in PrEC but not in PCa cells and this is due to the absence of a CCND1 3'-UTR in these cells. This suggests that miR-206-based anti-cyclin D1 targeted therapy would be beneficial in cancers where cyclin D1 is overexpressed and contains a 3'-UTR.

Identifiers

PMID25111862
PMCPMC5189965
OpenAlexW2002987011

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.