Evidence map›Paper›PMID 17460777›Full record

ArticleNeoplasia (New York, N.Y.)2007

Necrosis induction in glioblastoma cells reveals a new "bioswitch" function for the MT1-MMP/G6PT signaling axis in proMMP-2 activation versus cell death decision.

Anissa Belkaid, Simon Fortier, Jian Cao, Borhane Annabi

Open access · goldAbstract readComparative Study
In one paragraph

Article in Neoplasia (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Molecular Functions of Glycoconjugates in Autophagy.Journal of molecular biology · 2016
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Imaging hypoxia in gliomas.The British journal of radiology · 2011
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The War on Cancer rages on.Neoplasia (New York, N.Y.) · 2009
    Article
  18. Gliomas induce and exploit microglial MT1-MMP expression for tumor expansion.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

4 authors at 2 institutions in 2 countries.

Anissa BelkaidLaboratoire d'Oncologie Moléculaire, Département de Chimie, Centre BIOMED, Université du Québec à Montréal, Quebec, Canada.
Simon Fortier
Jian Cao
Borhane Annabi
Université du Québec à Montréal · CAState University of New York · US

Funding

Targeting the PEX Domain of MT1-MMP: Novel Cancer TherapyR01CA113553 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI CAO, JIAN · 2006 to 2010
$1.7M
NCI NIH HHS 1R01CA113553-01A1NCI NIH HHS R01 CA113553
6 · The paper itself

Abstract

Cytoskeleton disorganization is an early step in the activation process of matrix metalloproteinase 2 (MMP-2) by membrane type 1 MMP (MT1-MMP) but is also associated with endoplasmic reticulum (ER) dysfunction and subsequent cell death. Given evidence that the ER-embedded glucose-6-phosphate transporter (G6PT) regulates glioblastoma cell survival and that MT1-MMP is a key enzyme in the cancer cell invasive phenotype, we explored the molecular link between G6PT and MT1-MMP. Cytoskeleton-disrupting agents such as concanavalin A (ConA) and cytochalasin D triggered proMMP-2 activation and cell death in U87 glioma cells. ConA decreased G6PT gene expression, an event that was also observed in cells overexpressing the full-length recombinant MT1-MMP protein. Overexpression of a membrane-bound catalytically active but cytoplasmic domain-deleted MT1-MMP was unable to downregulate G6PT gene expression or to trigger necrosis. Gene silencing of MT1-MMP with small interfering RNA prevented proMMP-2 activation and induced G6PT gene expression. ConA inhibited Akt phosphorylation, whereas overexpression of recombinant G6PT rescued the cells from ConA-induced proMMP-2 activation and increased Akt phosphorylation. Altogether, new functions of MT1-MMP in cell death signaling may be linked to those of G6PT. Our study indicates a molecular signaling axis regulating the invasive phenotype of brain tumor cells and highlights a new "bioswitch" function for G6PT in cell survival.

Indexed as

Signal TransductionAntiportersBrain NeoplasmsCell DeathCell Line, TumorEnzyme ActivationEnzyme PrecursorsGelatinasesGlioblastomaHumansMatrix Metalloproteinase 14MetalloendopeptidasesMonosaccharide Transport ProteinsNecrosisNeoplasm ProteinsPhenotypeAntiportersEnzyme PrecursorsGelatinasesMatrix Metalloproteinase 14MetalloendopeptidasesMonosaccharide Transport ProteinsNeoplasm ProteinsprogelatinaseSLC37A4 protein, human

Identifiers

PMID17460777
PMCPMC1854846
OpenAlexW2148103638

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.