Evidence map›Paper›PMID 21317927›Full record

ArticleOncogene2011

MicroRNA-21 targets tumor suppressor genes ANP32A and SMARCA4.

K Schramedei, N Mörbt, G Pfeifer, J Läuter, M Rosolowski, J M Tomm, M von Bergen, F Horn, K Brocke-Heidrich

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Role of Chromatin-Associated RNAs in Eye Physiology and Pathology.Methods in molecular biology (Clifton, N.J.) · 2027
    Review
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  14. [Silenced ANP32A inhibits the growth, invasion and migration of colorectal cancerNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Gga-miR-181a modulates ANP32A expression and inhibits MDCC-MSB-1 cell.In vitro cellular & developmental biology. Animal · 2021
    Article

17 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

9 authors at 2 institutions in 1 country.

K SchramedeiInstitute of Clinical Immunology, Medical Faculty, University of Leipzig, Leipzig, Germany.
N Mörbt
G Pfeifer
J Läuter
M Rosolowski
J M Tomm
M von Bergen
F Horn
K Brocke-Heidrich
Leipzig University · DEHelmholtz Centre for Environmental Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA-21 (miR-21) is a key regulator of oncogenic processes. It is significantly elevated in the majority of human tumors and functionally linked to cellular proliferation, survival and migration. In this study, we used two experimental-based strategies to search for novel miR-21 targets. On the one hand, we performed a proteomic approach using two-dimensional differential gel electrophoresis (2D-DIGE) to identify proteins suppressed upon enhanced miR-21 expression in LNCaP human prostate carcinoma cells. The tumor suppressor acidic nuclear phosphoprotein 32 family, member A (ANP32A) (alias pp32 or LANP) emerged as the most strongly downregulated protein. On the other hand, we applied a mathematical approach to select correlated gene sets that are negatively correlated with primary-miR-21 (pri-miR-21) expression in published transcriptome data from 114 B-cell lymphoma cases. Among these candidates, we found tumor suppressor SMARCA4 (alias BRG1) together with the already validated miR-21 target, PDCD4. ANP32A and SMARCA4, which are both involved in chromatin remodeling processes, were confirmed as direct miR-21 targets by immunoblot analysis and reporter gene assays. Furthermore, knock down of ANP32A mimicked the effect of enforced miR-21 expression by enhancing LNCaP cell viability, whereas overexpression of ANP32A in the presence of high miR-21 levels abrogated the miR-21-mediated effect. In A172 glioblastoma cells, enhanced ANP32A expression compensated for the effects of anti-miR-21 treatment on cell viability and apoptosis. In addition, miR-21 expression clearly increased the invasiveness of LNCaP cells, an effect also seen in part upon downregulation of ANP32A. In conclusion, these results suggest that downregulation of ANP32A contributes to the oncogenic function of miR-21.

Indexed as

Base SequenceCells, CulturedCell SurvivalCell Transformation, NeoplasticDNA HelicasesDown-RegulationGene Expression RegulationGenes, Tumor SuppressorGene TargetingHumansIntracellular Signaling Peptides and ProteinsMicroRNAsMolecular Sequence DataNuclear ProteinsRegulatory Sequences, Ribonucleic AcidRNA-Binding ProteinsANP32A protein, humanDNA HelicasesIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN21 microRNA, humanNuclear ProteinsRegulatory Sequences, Ribonucleic AcidRNA-Binding ProteinsSMARCA4 protein, humanTranscription Factors

Identifiers

PMID21317927
PMCPMC3134876
OpenAlexW2024098388

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.