Evidence map›Paper›PMID 24497324›Full record

ArticleOncotarget2014

Role of miR-34a as a suppressor of L1CAM in endometrial carcinoma.

Uwe Schirmer, Kai Doberstein, Anne-Kathleen Rupp, Niko P Bretz, Daniela Wuttig, Helena Kiefel, Christian Breunig, Heidi Fiegl, Elisabeth Müller-Holzner, Robert Zeillinger and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Non-Coding RNAs as Prognostic Markers for Endometrial Cancer.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Endometrial cancer prognosis correlates with the expression of L1CAM and miR34a biomarkers.Journal of experimental & clinical cancer research : CR · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. MicroRNAs: new players in cataract.American journal of translational research · 2017
    Review
  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

14 authors at 5 institutions in 2 countries.

Uwe SchirmerDepartment of Translational Immunology, German Cancer Research Center.
Kai Doberstein
Anne-Kathleen Rupp
Niko P Bretz
Daniela Wuttig
Helena Kiefel
Christian Breunig
Heidi Fiegl
Elisabeth Müller-Holzner
Robert Zeillinger
Eva Schuster
Alain G Zeimet
Holger Sültmann
Peter Altevogt
German Cancer Research Center · DEMedical University of Vienna · ATUniversität Innsbruck · ATHeidelberg University · DEInnsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

L1CAM promotes cell motility, invasion and metastasis formation in various human cancers and can be considered as a driver of tumor progression. Knowledge about genetic processes leading to the presence of L1CAM in cancers is of considerable importance. Experimentally, L1CAM expression can be achieved by various means. Over-expression of the transcription factor SLUG or treatment of cells with TGF-β1 can induce or augment L1CAM levels in cancer cells. Likewise, hypomethylation of the L1CAM promoter on the X chromosome correlates with L1CAM expression. However, presently no mechanisms that might control transcriptional activity are known. Here we have identified miR-34a as a suppressor of L1CAM. We observed that L1CAM positive endometrial carcinoma (EC) cell lines HEC1B and SPAC1L lost L1CAM protein and mRNA by treatment with demethylating agents or knock-down of the DNA-methyltransferase-1 (DNMT1). Concomitantly, several miRNAs were up-regulated. Using miRNA profiling, luciferase reporter assays and mutagenesis, we identified miR-34a as a putative binder to the L1CAM-3'UTR. Over-expression of miR-34a in HEC1B cells blocked L1CAM expression and inhibited cell migration. In ECC1 cells (wildtype p53) the activation of p53 caused miR-34a up-regulation and loss of L1CAM expression that was miR-34a dependent. We observed an inverse correlation between L1CAM and miR-34a levels in EC cell lines. In primary tumor sections areas expressing high amounts of L1CAM had less miR-34a expression than those with low L1CAM levels. Our data suggest that miR-34a can regulate L1CAM expression by targeting L1CAM mRNA for degradation. These findings shed new light on the complex regulation of L1CAM in human tumors.

Indexed as

3' Untranslated RegionsAzacitidineBase SequenceCell Growth ProcessesCell Line, TumorCell MovementEndometrial NeoplasmsFemaleHumansImidazolesMicroRNAsMolecular Sequence DataNeural Cell Adhesion Molecule L1PiperazinesTranscriptional ActivationTranscription Factors3' Untranslated RegionsAzacitidineImidazolesMicroRNAsMIRN34 microRNA, humanNeural Cell Adhesion Molecule L1nutlin 3PiperazinesTranscription Factors

Identifiers

PMID24497324
PMCPMC3964221
OpenAlexW1502740750

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.