Evidence map›Paper›PMID 31238903›Full record

ArticleBMC cancer2019

miR-221-5p regulates proliferation and migration in human prostate cancer cells and reduces tumor growth in vivo.

Mirjam Kiener, Lanpeng Chen, Markus Krebs, Joël Grosjean, Irena Klima, Charis Kalogirou, Hubertus Riedmiller, Burkhard Kneitz, George N Thalmann, Ewa Snaar-Jagalska and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-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

31 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Computational and structural biotechnology journal · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

13 authors at 3 institutions in 3 countries.

Mirjam KienerUrology Research Laboratory, Department for BioMedical Research, University of Bern, Bern, Switzerland.
Lanpeng ChenIBL, University of Leiden, Leiden, the Netherlands.
Markus KrebsDepartment of Urology and Paediatric Urology, University Medical Center of Würzburg, Würzburg, Germany.
Joël GrosjeanUrology Research Laboratory, Department for BioMedical Research, University of Bern, Bern, Switzerland.
Irena KlimaUrology Research Laboratory, Department for BioMedical Research, University of Bern, Bern, Switzerland.
Charis KalogirouDepartment of Urology and Paediatric Urology, University Medical Center of Würzburg, Würzburg, Germany.
Hubertus RiedmillerDepartment of Urology and Paediatric Urology, University Medical Center of Würzburg, Würzburg, Germany.
Burkhard KneitzDepartment of Urology and Paediatric Urology, University Medical Center of Würzburg, Würzburg, Germany.
George N ThalmannUrology Research Laboratory, Department for BioMedical Research, University of Bern, Bern, Switzerland.
Ewa Snaar-JagalskaIBL, University of Leiden, Leiden, the Netherlands.
Martin SpahnUrology Center Zürich, Clinic Hirslanden, Zürich, Switzerland.
Marianna Kruithof-de JulioUrology Research Laboratory, Department for BioMedical Research, University of Bern, Bern, Switzerland. marianna.kruithofdejulio@dbmr.unibe.ch.
Eugenio ZoniUrology Research Laboratory, Department for BioMedical Research, University of Bern, Bern, Switzerland. eugenio.zoni@dbmr.unibe.ch.ORCID http://orcid.org/0000-0002-3070-7694
University of Bern · CHLeiden University · NLKlinik Hirslanden · CH

Funding

Deutsche Forschungsgemeinschaft 269025972Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 310030L_156905Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung 31003A_169352
6 · The paper itself

Abstract

backgroundDespite latest advances in prostate cancer (PCa) therapy, PCa remains the third-leading cause of cancer-related death in European men. Dysregulation of microRNAs (miRNAs), small non-coding RNA molecules with gene expression regulatory function, has been reported in all types of epithelial and haematological cancers. In particular, miR-221-5p alterations have been reported in PCa.

methodsmiRNA expression data was retrieved from a comprehensive publicly available dataset of 218 PCa patients (GSE21036) and miR-221-5p expression levels were analysed. The functional role of miR-221-5p was characterised in androgen- dependent and androgen- independent PCa cell line models (C4-2 and PC-3M-Pro4 cells) by miR-221-5p overexpression and knock-down experiments. The metastatic potential of highly aggressive PC-3M-Pro4 cells overexpressing miR-221-5p was determined by studying extravasation in a zebrafish model. Finally, the effect of miR-221-5p overexpression on the growth of PC-3M-Pro4luc2 cells in vivo was studied by orthotopic implantation in male Balb/cByJ nude mice and assessment of tumor growth.

resultsAnalysis of microRNA expression dataset for human primary and metastatic PCa samples and control normal adjacent benign prostate revealed miR-221-5p to be significantly downregulated in PCa compared to normal prostate tissue and in metastasis compared to primary PCa. Our in vitro data suggest that miR-221-5p overexpression reduced PCa cell proliferation and colony formation. Furthermore, miR-221-5p overexpression dramatically reduced migration of PCa cells, which was associated with differential expression of selected EMT markers. The functional changes of miR-221-5p overexpression were reversible by the loss of miR-221-5p levels, indicating that the tumor suppressive effects were specific to miR-221-5p. Additionally, miR-221-5p overexpression significantly reduced PC-3M-Pro4 cell extravasation and metastasis formation in a zebrafish model and decreased tumor burden in an orthotopic mouse model of PCa.

conclusionsTogether these data strongly support a tumor suppressive role of miR-221-5p in the context of PCa and its potential as therapeutic target.

Indexed as

Analysis of VarianceAnimalsCell Line, TumorCell MovementCell ProliferationDown-RegulationGene Knockdown TechniquesHumansMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsNeoplasm MetastasisProstateProstatic NeoplasmsMicroRNAsMIR221, humanMigrationmiR-221-5pProliferationProstate cancerTumor suppressor miRNA

Identifiers

PMID31238903
PMCPMC6593572
OpenAlexW2955080905

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.