Evidence map›Paper›PMID 24098452›Full record

ArticlePloS one2013

miR-125b acts as a tumor suppressor in breast tumorigenesis via its novel direct targets ENPEP, CK2-α, CCNJ, and MEGF9.

Andrea Feliciano, Josep Castellvi, Ana Artero-Castro, Jose A Leal, Cleofé Romagosa, Javier Hernández-Losa, Vicente Peg, Angels Fabra, Francisco Vidal, Hiroshi Kondoh and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
7.5field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 149 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.International journal of molecular sciences · 2026
    Article
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  12. Landscape of NcRNAs involved in drug resistance of breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  13. Review
  14. miR-125b-5p, miR-155-3p, and miR-214-5p and TargetInternational journal of molecular sciences · 2023
    Article
  15. Article
  16. Article
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  18. Article
  19. Review
  20. Article

27 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Andrea FelicianoOncology and Molecular Pathology Group, Pathology Department, Institut de Recerca Hospital Vall d'Hebron, Barcelona, Spain.
Josep Castellvi
Ana Artero-Castro
Jose A Leal
Cleofé Romagosa
Javier Hernández-Losa
Vicente Peg
Angels Fabra
Francisco Vidal
Hiroshi Kondoh
Santiago Ramón Y Cajal
Matilde E Lleonart
Vall d'Hebron Institut de Recerca · ESBanc de Sang i Teixits · ESInstitut d'Investigació Biomédica de Bellvitge · ESKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) play important roles in diverse biological processes and are emerging as key regulators of tumorigenesis and tumor progression. To explore the dysregulation of miRNAs in breast cancer, a genome-wide expression profiling of 939 miRNAs was performed in 50 breast cancer patients. A total of 35 miRNAs were aberrantly expressed between breast cancer tissue and adjacent normal breast tissue and several novel miRNAs were identified as potential oncogenes or tumor suppressor miRNAs in breast tumorigenesis. miR-125b exhibited the largest decrease in expression. Enforced miR-125b expression in mammary cells decreased cell proliferation by inducing G2/M cell cycle arrest and reduced anchorage-independent cell growth of cells of mammary origin. miR-125b was found to perform its tumor suppressor function via the direct targeting of the 3'-UTRs of ENPEP, CK2-α, CCNJ, and MEGF9 mRNAs. Silencing these miR-125b targets mimicked the biological effects of miR-125b overexpression, confirming that they are modulated by miR-125b. Analysis of ENPEP, CK2-α, CCNJ, and MEGF9 protein expression in breast cancer patients revealed that they were overexpressed in 56%, 40-56%, 20%, and 32% of the tumors, respectively. The expression of ENPEP and CK2-α was inversely correlated with miR-125b expression in breast tumors, indicating the relevance of these potential oncogenic proteins in breast cancer patients. Our results support a prognostic role for CK2-α, whose expression may help clinicians predict breast tumor aggressiveness. In particular, our results show that restoration of miR-125b expression or knockdown of ENPEP, CK2-α, CCNJ, or MEGF9 may provide novel approaches for the treatment of breast cancer.

Indexed as

Genes, Tumor Suppressor3' Untranslated RegionsBreast NeoplasmsCasein Kinase IICell LineCell ProliferationCell Transformation, NeoplasticCluster AnalysisCyclinsFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlutamyl AminopeptidaseHumansMembrane Proteins3' Untranslated RegionsCasein Kinase IICCNJ protein, humanCyclinsENPEP protein, humanGlutamyl AminopeptidaseMEGF9 protein, humanMembrane ProteinsMicroRNAsMIRN125 microRNA, humanNerve Tissue Proteins

Identifiers

PMID24098452
PMCPMC3789742
OpenAlexW1997421768

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.