Evidence map›Paper›PMID 18978811›Full record

ArticleOncogene2009

Suppression of neuroblastoma growth by dipeptidyl peptidase IV: relevance of chemokine regulation and caspase activation.

W T Arscott, A E LaBauve, V May, U V Wesley

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

30 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Galectin-3 protects against ischemic stroke by promoting neuro-angiogenesis via apoptosis inhibition and Akt/Caspase regulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  10. Article
  11. Article
  12. CD26 and Asthma: a Comprehensive Review.Clinical reviews in allergy & immunology · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. DPPIV/CD26: a tumor suppressor or a marker of malignancy?Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  19. Article
  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 1 institution in 1 country.

W T ArscottDepartment of Microbiology and Molecular Genetics, Vermont Cancer Center, University of Vermont, Burlington, VT 05405, USA.
A E LaBauve
V May
U V Wesley
University of Vermont · US

Funding

Proteomics Core for Neuroscience P20 RR16435P20RR016435 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI MARTIN-CARABALLO, MIGUEL · 2001 to 2010
$23.5M
NCRR NIH HHS 2 P20 RR016435-P4Y6NCRR NIH HHS P20 RR016435
6 · The paper itself

Abstract

Imbalanced protease expression and activities may contribute to the development of cancers, including neuroblastoma (NB). NB is a fatal childhood cancer of the sympathetic nervous system that frequently overexpresses mitogenic peptides, chemokines and their receptors. Dipeptidyl peptidase IV (DPPIV), a cell surface serine protease, inactivates or degrades some of these bioactive peptides and chemokines, thereby regulating cell proliferation and survival. Our studies show that DPPIV is expressed in normal neural crest-derived structures, including superior cervical and dorsal root ganglion cells, sciatic nerve, and in adrenal glands, but its expression is greatly decreased or lost in cells derived from NB, their malignant counterpart. Restoration of DPPIV expression in NB cells led to their differentiation in association with increased expression of the neural marker MAP2 and decreased expression of chemokines, including stromal-derived factor 1 (SDF1) and its receptor CXCR4. Furthermore, DPPIV promoted apoptosis, and inhibited SDF1-mediated in vitro cell migration and angiogenic potential. These changes were accompanied by caspase activation and decreased levels of phospho-Akt and MMP9 activity, which are downstream effectors of SDF1-CXCR4 signaling. Importantly, DPPIV suppressed the tumorigenic potential of NB cells in a xenotransplantation mouse model. These data support a potential role for DPPIV in inhibiting NB growth and progression.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntigens, DifferentiationApoptosisCaspasesCell DifferentiationCell Line, TumorCell MovementCell ProliferationCell SurvivalChemokine CXCL12Dipeptidyl Peptidase 4Enzyme ActivationGrowth SubstancesMatrix Metalloproteinase 9MiceAntigens, DifferentiationCaspasesChemokine CXCL12Cxcr4 protein, ratDipeptidyl Peptidase 4Growth SubstancesMAP2 protein, ratMatrix Metalloproteinase 9Microtubule-Associated ProteinsMtap2 protein, mouseProto-Oncogene Proteins c-aktReceptors, CXCR4

Identifiers

PMID18978811
PMCPMC2633428
OpenAlexW2090339110

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.