Evidence map›Paper›PMID 22956186›Full record

ArticleAngiogenesis2013

Notch signaling regulates tumor-induced angiogenesis in SPARC-overexpressed neuroblastoma.

Bharathi Gorantla, Praveen Bhoopathi, Chandramu Chetty, Venkateswara Rao Gogineni, G S Sailaja, Christopher S Gondi, Jasti S Rao

Abstract read
In one paragraph

Article in Angiogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Natural products against cancer angiogenesis.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

7 authors.

Bharathi GorantlaDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, IL 61605, USA.
Praveen Bhoopathi
Chandramu Chetty
Venkateswara Rao Gogineni
G S Sailaja
Christopher S Gondi
Jasti S Rao

Funding

Combination therapy to inhibit neuroblastoma growthR01CA147792 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GONDI, CHRISTOPHER SUMEET BABU · 2010 to 2014
$1.6M
NCI NIH HHS CA147792NCI NIH HHS R01 CA147792
6 · The paper itself

Abstract

Despite existing aggressive treatment modalities, the prognosis for advanced stage neuroblastoma remains poor with significant long-term illness in disease survivors. Advance stage disease features are associated with tumor vascularity, and as such, angiogenesis inhibitors may prove useful along with current therapies. The matricellular protein, secreted protein acidic and rich in cysteine (SPARC), is known to inhibit proliferation and migration of endothelial cells stimulated by growth factors. Here, we sought to determine the effect of SPARC on neuroblastoma tumor cell-induced angiogenesis and to decipher the molecular mechanisms involved in angiogenesis inhibition. Conditioned medium from SPARC-overexpressed neuroblastoma cells (pSPARC-CM) inhibited endothelial tube formation, cell proliferation, induced programmed cell death and suppressed expression of pro-angiogenic molecules such as VEGF, FGF, PDGF, and MMP-9 in endothelial cells. Further analyses revealed that pSPARC-CM-suppressed expression of growth factors was mediated by inhibition of the Notch signaling pathway, and cells cultured on conditioned medium from tumor cells that overexpress both Notch intracellular domain (NICD-CM) and SPARC resumed the pSPARC-CM-suppressed capillary tube formation and growth factor expression in vitro. Further, SPARC overexpression in neuroblastoma cells inhibited neo-vascularization in vivo in a mouse dorsal air sac model. Furthermore, SPARC overexpression-induced endothelial cell death was observed by co-localization studies with TUNEL assay and an endothelial marker, CD31, in xenograft tumor sections from SPARC-overexpressed mice. Our data collectively suggest that SPARC overexpression induces endothelial cell apoptosis and inhibits angiogenesis both in vitro and in vivo.

Indexed as

Signal TransductionAngiogenesis Inducing AgentsAnimalsApoptosisCell Line, TumorCell ProliferationCell SurvivalCulture Media, ConditionedDisease Models, AnimalEndothelial CellsHumansMiceMice, NudeNeovascularization, PathologicNeuroblastomaOsteonectinAngiogenesis Inducing AgentsCulture Media, ConditionedOsteonectinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, NotchSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID22956186
PMCPMC3527677

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Registered trials

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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.