Evidence map›Paper›PMID 25915824›Full record

ArticleLeukemia2015

MicroRNA-124 links p53 to the NF-κB pathway in B-cell lymphomas.

D Jeong, J Kim, J Nam, H Sun, Y-H Lee, T-J Lee, R C T Aguiar, S-W Kim

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. MicroRNAs in atopic dermatitis: A systematic review.Journal of cellular and molecular medicine · 2020
    Pooled it
  2. Review
  3. Article
  4. Article
  5. The Role of MicroRNA in the Pathogenesis of Atopic Dermatitis.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Role of p53 in Regulating Radiation Responses.Life (Basel, Switzerland) · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 2 countries.

D JeongDepartment of Biological Sciences, Pusan National University, Pusan, Korea.
J KimDepartment of Biological Sciences, Pusan National University, Pusan, Korea.
J NamDepartment of Biological Sciences, Pusan National University, Pusan, Korea.
H SunDepartment of Statistics, Pusan National University, Pusan, Korea.
Y-H LeeDepartment of Radiation Oncology, Yonsei University, Seoul, Korea.
T-J LeeDepartment of Anatomy, Yeungnam University, Daegu, Korea.
R C T AguiarDivision of Hematology and Medical Oncology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
S-W KimDepartment of Biological Sciences, Pusan National University, Pusan, Korea.
Pusan National University · KRThe University of Texas Health Science Center at San Antonio · USYeungnam University · KRYonsei University · KR

Funding

microRNA-155 and LymphomaR01CA138747 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AGUIAR, RICARDO C · 2010 to 2014
$1.5M
Post-Translational Control of TET Function in LymphomaI01BX001882 · VA · SOUTH TEXAS VETERANS HEALTH CARE SYSTEM · PI AGUIAR, RICARDO C · 2013 to 2025
–
BLRD VA I01 BX001882Intramural NIH HHSNCI NIH HHS R01-CA138747
6 · The paper itself

Abstract

The contribution of microRNAs to lymphoma biology is not fully understood. In particular, it remains untested whether microRNA dysregulation could contribute to the emergence of the aggressive subset of B-cell lymphomas that coexpress MYC and BCL2. Here, we identify microRNA-124 (miR-124) as a negative regulator of MYC and BCL2 expression in B-cell lymphomas. Concordantly, stable or transient ectopic expression of miR-124 suppressed cell proliferation and survival, whereas genetic inhibition of this miRNA enhanced the fitness of these tumors. Mechanistically, the activities of miR-124 towards MYC and BCL2 intersect with both oncogenic and tumor-suppressive pathways. In respect to the former, we show that miR-124 directly targets nuclear factor-κB (NF-κB) p65, and using genetic approaches, we demonstrate that this interaction accounts for the miR-124-mediated suppression of MYC and BCL2. We also characterized miR-124 promoter region and identified a functional p53 binding site. In agreement with this finding, endogenous or ectopic expression of wild-type, but not mutant, p53 increased miR-124 levels and suppressed p65, MYC and BCL2. Our data unveil an miRNA-dependent regulatory circuitry that links p53 to the NF-κB pathway, which when disrupted in B-cell lymphoma may be associated with aberrant coexpression of MYC and BCL2 and poor prognosis.

Indexed as

Gene Expression Regulation, NeoplasticSignal Transduction3' Untranslated RegionsApoptosisCell Line, TumorCell ProliferationCell SurvivalCloning, MolecularGene ExpressionGenes, bcl-2Genes, mycGenes, ReporterHumansLymphoma, B-CellMicroRNAsMutagenesis, Site-Directed3' Untranslated RegionsMicroRNAsMIRN124 microRNA, humanNF-kappa BTranscription Factor RelATumor Suppressor Protein p53

Identifiers

PMID25915824
OpenAlexW2071248529

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.