Evidence map›Paper›PMID 18350569›Full record

ArticleInternational journal of cancer2008

SPARC-induced increase in glioma matrix and decrease in vascularity are associated with reduced VEGF expression and secretion.

Christopher K Yunker, William Golembieski, Nancy Lemke, Chad R Schultz, Simona Cazacu, Chaya Brodie, Sandra A Rempel

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.5field-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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  3. Secretome profiling ofFrontiers in oncology · 2023
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  14. Re-sensitization of 5-FU resistance by SPARC through negative regulation of glucose metabolism in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

7 authors at 1 institution in 1 country.

Christopher K YunkerBarbara Jane Levy Laboratory of Molecular Neuro-Oncology, Hermelin Brain Tumor Center, Department of Neurosurgery, Henry Ford Hospital, Detroit, MI 48202, USA.
William Golembieski
Nancy Lemke
Chad R Schultz
Simona Cazacu
Chaya Brodie
Sandra A Rempel
Henry Ford Hospital · US

Funding

THE ROLE OF SPARC IN GLIOMA INVASIONR01CA086997 · NCI · HENRY FORD HEALTH SYSTEM · PI REMPEL, SANDRA ANN · 2001 to 2007
$1.8M
Regulation of Glioma Cell Apoptosis in PKCDeltaR01CA109196 · NCI · HENRY FORD HEALTH SYSTEM · PI BRODIE, CHAYA · 2005 to 2008
$991k
NCI NIH HHS CA086997NCI NIH HHS CA109196NCI NIH HHS R01 CA086997
6 · The paper itself

Abstract

Glioblastomas are heterogeneous tumors displaying regions of necrosis, proliferation, angiogenesis, apoptosis and invasion. SPARC, a matricellular protein that negatively regulates angiogenesis and cell proliferation, but enhances cell deadhesion from matrix, is upregulated in gliomas (Grades II-IV). We previously demonstrated that SPARC promotes invasion while concomitantly decreasing tumor growth, in part by decreasing proliferation of the tumor cells. In other cancer types, SPARC has been shown to influence tumor growth by altering matrix production, and by decreasing angiogenesis via interfering with the VEGF-VEGFR1 signaling pathway. We therefore examined whether the SPARC-induced decrease in glioma tumor growth was also, in part, due to alterations in matrix and/or decreased vascularity, and assessed SPARC-VEGF interactions. The data demonstrate that SPARC upregulates glioma matrix, collagen I is a constituent of the matrix and SPARC promotes collagen fibrillogenesis. Furthermore, SPARC suppressed glioma vascularity, and this was accompanied by decreased VEGF expression and secretion, which was, in part, due to reduced VEGF165 transcript abundance. These data indicate that SPARC modulates glioma growth by altering the tumor microenvironment and by suppressing tumor vascularity through suppression of VEGF expression and secretion. These experiments implicate a novel mechanism, whereby SPARC regulates VEGF function by limiting the available growth factor. Because SPARC is considered to be a therapeutic target for gliomas, a further understanding of its complex signaling mechanisms is important, as targeting SPARC to decrease invasion could undesirably lead to the growth of more vascular and proliferative tumors.

Indexed as

AnimalsBase SequenceBrain NeoplasmsCell Line, TumorCollagen Type IDNA PrimersGliomaImmunohistochemistryImmunoprecipitationOsteonectinRatsReverse Transcriptase Polymerase Chain ReactionVascular Endothelial Growth Factor ACollagen Type IDNA PrimersOsteonectinVascular Endothelial Growth Factor A

Identifiers

PMID18350569
PMCPMC3644882
OpenAlexW2047335027

What OpenQuestion holds

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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.