Evidence map›Paper›PMID 29094504›Full record

ArticleMolecular oncology2018

A link between the fibroblast growth factor axis and the miR-16 family reveals potential new treatment combinations in mesothelioma.

Karin Schelch, Michaela B Kirschner, Marissa Williams, Yuen Y Cheng, Nico van Zandwijk, Michael Grusch, Glen Reid

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Novel and Future Treatment Options in Mesothelioma: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Aberrant Expression of FGFRL1 in Esophageal Cancer and Its Regulation by miR-107.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Genomics and Functional Genomics of Malignant Pleural Mesothelioma.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

7 authors at 4 institutions in 3 countries.

Karin SchelchAsbestos Diseases Research Institute, Sydney, Australia.ORCID 0000-0001-8742-1737
Michaela B KirschnerAsbestos Diseases Research Institute, Sydney, Australia.
Marissa WilliamsAsbestos Diseases Research Institute, Sydney, Australia.
Yuen Y ChengAsbestos Diseases Research Institute, Sydney, Australia.
Nico van ZandwijkAsbestos Diseases Research Institute, Sydney, Australia.
Michael GruschDepartment of Medicine I, Institute of Cancer Research, Medical University of Vienna, Austria.
Glen ReidAsbestos Diseases Research Institute, Sydney, Australia.
Asbestos Diseases Research Institute · AUComprehensive Cancer Center Vienna · ATThe University of Sydney · AUUniversity Hospital of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant pleural mesothelioma (MPM) is an aggressive malignancy with very limited therapeutic options. Fibroblast growth factor (FGF) signals play important roles in mesothelioma cell growth. Several FGFs and FGF receptors (FGFRs) are predicted targets of the miR-15/16 family, which is downregulated in MPM. The aim of this study was to explore the link between the miR-15/16 family and the FGF axis in MPM. Expression analyses via RT-qPCR showed downregulation of the FGF axis after transfection with miR-15/16 mimics. Direct interaction was confirmed by luciferase reporter assays. Restoration of miR-15/16 led to dose-dependent growth inhibition in MPM cell lines, which significantly correlated with their sensitivity to FGFR inhibition. Treatment with recombinant FGF2 prevented growth inhibition and further reduced the levels of FGF/R-targeting microRNAs, indicating a vicious cycle between miR-15/16 down- and FGF/FGFR signaling upregulation. Combined inhibition of two independent miR-15/16 targets, the FGF axis and Bcl-2, resulted in additive or synergistic activity. Our data indicate that post-transcriptional repression of FGF-mediated signals contributes to the tumor suppressor function of the microRNA-15/16 family. Inhibiting hyperactivated FGF signals and Bcl-2 might serve as a novel therapeutic combination strategy in MPM.

Indexed as

Cell Line, TumorDown-RegulationFibroblast Growth Factor 2Fibroblast Growth FactorsHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantMicroRNAsPleuraProto-Oncogene Proteins c-bcl-2Receptors, Fibroblast Growth FactorRecombinant ProteinsUp-RegulationFibroblast Growth Factor 2Fibroblast Growth FactorsMicroRNAsMIRN15 microRNA, humanMIRN16 microRNA, humanProto-Oncogene Proteins c-bcl-2Receptors, Fibroblast Growth FactorRecombinant Proteinsfibroblast growth factor, fibroblast growth factor receptormalignant pleural mesotheliomamicroRNA-15microRNA-16

Identifiers

PMID29094504
PMCPMC5748487
OpenAlexW2766689053

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.