Evidence map›Paper›PMID 27541285›Full record

ArticleMolecular neurobiology2017

Metalloproteinases ADAM10 and ADAM17 Mediate Migration and Differentiation in Glioblastoma Sphere-Forming Cells.

Elodie J Siney, Alexander Holden, Elizabeth Casselden, Harry Bulstrode, Gareth J Thomas, Sandrine Willaime-Morawek

Open access · hybridAbstract read
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Proteomic profiling of CD133 + and CD326 + (EpCAM) subpopulations in A549 cells: insights into pluripotency and tumor heterogeneity.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  12. Proteases Regulate Cancer Stem Cell Properties and Remodel Their Microenvironment.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
  13. Systematic analysis of potential targets of the curcumin analog pentagamavunon-1 (PGV-1) in overcoming resistance of glioblastoma cells to bevacizumab.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021
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  19. The metalloprotease ADAM10 (a disintegrin and metalloprotease 10) undergoes rapid, postlysis autocatalytic degradation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
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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

6 authors at 2 institutions in 1 country.

Elodie J SineyClinical Neurosciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK. ejs304@soton.ac.uk.
Alexander HoldenClinical Neurosciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Elizabeth CasseldenClinical Neurosciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Harry BulstrodeWessex Neurological Centre, University Hospital Southampton, Southampton, SO16 6YD, UK.
Gareth J ThomasCancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Sandrine Willaime-MorawekClinical Neurosciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
University of Southampton · GBUniversity Hospital Southampton NHS Foundation Trust · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

Glioblastoma is the most common form of primary malignant brain tumour. These tumours are highly proliferative and infiltrative resulting in a median patient survival of only 14 months from diagnosis. The current treatment regimens are ineffective against the small population of cancer stem cells residing in the tumourigenic niche; however, a new therapeutic approach could involve the removal of these cells from the microenvironment that maintains the cancer stem cell phenotype. We have isolated multipotent sphere-forming cells from human high grade glioma (glioma sphere-forming cells (GSCs)) to investigate the adhesive and migratory properties of these cells in vitro. We have focused on the role of two closely related metalloproteinases ADAM10 and ADAM17 due to their high expression in glioblastoma and GSCs and their ability to activate cytokines and growth factors. Here, we report that ADAM10 and ADAM17 inhibition selectively increases GSC, but not neural stem cell, migration and that the migrated GSCs exhibit a differentiated phenotype. We also observed a correlation between nestin, a stem/progenitor marker, and fibronectin, an extracellular matrix protein, expression in high grade glioma tissues. GSCs adherence on fibronectin is mediated by α5β1 integrin, where fibronectin further promotes GSC migration and is an effective candidate for in vivo cancer stem cell migration out of the tumourigenic niche. Our results suggest that therapies against ADAM10 and ADAM17 may promote cancer stem cell migration away from the tumourigenic niche resulting in a differentiated phenotype that is more susceptible to treatment.

Indexed as

Cell MovementADAM10 ProteinADAM17 ProteinAdultAgedCell DeathCell DifferentiationExtracellular MatrixFemaleFibronectinsGlioblastomaHumansIntegrin alpha5beta1MaleMatrix Metalloproteinase InhibitorsMiddle AgedADAM10 ProteinADAM17 ProteinFibronectinsIntegrin alpha5beta1Matrix Metalloproteinase InhibitorsCancer stem cellCell differentiationCell migrationDisintegrinExtracellular matrixGlioma

Identifiers

PMID27541285
PMCPMC5443867
OpenAlexW2513561817

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.