Evidence map›Paper›PMID 23619303›Full record

ArticleMolecular cancer therapeutics2013

Identification and characterization of a small-molecule inhibitor of Wnt signaling in glioblastoma cells.

Alessandra De Robertis, Silvia Valensin, Marco Rossi, Patrizia Tunici, Margherita Verani, Antonella De Rosa, Cinzia Giordano, Maurizio Varrone, Arianna Nencini, Carmela Pratelli and 13 more

Open access · greenAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. DKK3 Expression in Glioblastoma: Correlations with Biomolecular Markers.International journal of molecular sciences · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Frontiers in physiology · 2018
    Review
  18. WNT Signaling in Cardiac and Vascular Disease.Pharmacological reviews · 2018
    Review
  19. Targeting WNT Signaling for Multifaceted Glioblastoma Therapy.Frontiers in cellular neuroscience · 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

23 authors at 3 institutions in 2 countries.

Alessandra De RobertisCorresponding Author: Massimiliano Salerno, Siena Biotech Medicine Research Centre, Via del Petriccio e Belriguardo 35, 53100, Siena, Italy. msalerno@sienabiotech.it.
Silvia Valensin
Marco Rossi
Patrizia Tunici
Margherita Verani
Antonella De Rosa
Cinzia Giordano
Maurizio Varrone
Arianna Nencini
Carmela Pratelli
Tiziana Benicchi
Annette Bakker
Jeffrey Hill
Kanda Sangthongpitag
Vishal Pendharkar
Boping Liu
Fui Mee Ng
Siew Wen Then
Shi Jing Tai
Seong-Moon Cheong
Xi He
Andrea Caricasole
Massimiliano Salerno
Siena Biotech (Italy) · ITAgency for Science, Technology and Research · SGExperimental Drug Development Centre · SG

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI CHEN, CHINFEI · 1985 to 2015
$26.2M
Wnt-LRP interaction in Wnt signal transductionR01GM057603 · NIGMS · CHILDREN'S HOSPITAL BOSTON · PI HE, XI · 1999 to 2018
$6.3M
Genetic and Chemical Biological Studies of a Novel Wnt Inhibitor Tiki2R01AR060359 · NIAMS · BOSTON CHILDREN'S HOSPITAL · PI HE, XI · 2011 to 2015
$2.8M
Wnt/beta-catenin signaling: phosphorylation regulation of Wnt receptor-Axin interR01GM074241 · NIGMS · CHILDREN'S HOSPITAL BOSTON · PI HE, XI · 2005 to 2013
$2.5M
NIAMS NIH HHS R01 AR060359NICHD NIH HHS P30 HD018655NIGMS NIH HHS R01 GM057603NIGMS NIH HHS R01 GM074241
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common and prognostically unfavorable form of brain tumor. The aggressive and highly invasive phenotype of these tumors makes them among the most anatomically damaging human cancers with a median survival of less than 1 year. Although canonical Wnt pathway activation in cancers has been historically linked to the presence of mutations involving key components of the pathway (APC, β-catenin, or Axin proteins), an increasing number of studies suggest that elevated Wnt signaling in GBM is initiated by several alternative mechanisms that are involved in different steps of the disease. Therefore, inhibition of Wnt signaling may represent a therapeutically relevant approach for GBM treatment. After the selection of a GBM cell model responsive to Wnt inhibition, we set out to develop a screening approach for the identification of compounds capable of modulating canonical Wnt signaling and associated proliferative responses in GBM cells. Here, we show that the small molecule SEN461 inhibits the canonical Wnt signaling pathway in GBM cells, with relevant effects at both molecular and phenotypic levels in vitro and in vivo. These include SEN461-induced Axin stabilization, increased β-catenin phosphorylation/degradation, and inhibition of anchorage-independent growth of human GBM cell lines and patient-derived primary tumor cells in vitro. Moreover, in vivo administration of SEN461 antagonized Wnt signaling in Xenopus embryos and reduced tumor growth in a GBM xenograft model. These data represent the first demonstration that small-molecule-mediated inhibition of Wnt signaling may be a potential approach for GBM therapeutics.

Indexed as

AnimalsAntineoplastic AgentsBrain NeoplasmsCell Line, TumorCell ProliferationFemaleGlioblastomaHEK293 CellsHeterocyclic Compounds, 3-RingHumansMiceMice, NudePrognosisSignal TransductionTransfectionWnt Signaling PathwayAntineoplastic AgentsHeterocyclic Compounds, 3-RingXAV939

Identifiers

PMID23619303
PMCPMC3707945
OpenAlexW2133505501

What OpenQuestion holds

Textmetadata
LicenceTDM
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.