Evidence map›Paper›PMID 21918972›Full record

ArticleInternational journal of cancer2012

KSHV activation of VEGF secretion and invasion for endothelial cells is mediated through viral upregulation of emmprin-induced signal transduction.

Lu Dai, Momka Bratoeva, Bryan P Toole, Zhiqiang Qin, Chris Parsons

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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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

5 authors at 4 institutions in 2 countries.

Lu DaiDepartment of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, SC, USA.
Momka Bratoeva
Bryan P Toole
Zhiqiang Qin
Chris Parsons
MUSC Hollings Cancer Center · USIn-Q-Tel · USMedical University of South Carolina · USTongji University · CN

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
THE ROLE OF THE RNA BINDING PROTEIN LA IN ORAL TUMOR BIOLOGYP20RR017696 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SOMMER, GUNHILD · 2002 to 2011
$20.7M
SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
South Carolina Clinical & Translational Research Institute (SCTR)UL1TR000062 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2012 to 2014
$9.4M
PERTURBATION OF HYALURONAN FUNCTION IN CANCERR01CA082867 · NCI · TUFTS UNIVERSITY BOSTON · PI TOOLE, BRYAN P · 1999 to 2010
$2.1M
Regulation of the Tumor Microenvironment by KSHVR01CA142362 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI PARSONS, CHRISTOPHER H · 2010 to 2014
$1.4M
NCATS NIH HHS UL1 TR000062NCI NIH HHS CA082867NCI NIH HHS P30 CA138313NCI NIH HHS P30-CA-138313NCI NIH HHS R01 CA082867NCI NIH HHS R01 CA142362NCI NIH HHS R01-CA142362NCRR NIH HHS P20 RR017696NCRR NIH HHS P20-RR-017696NCRR NIH HHS UL1 RR029882
6 · The paper itself

Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi's sarcoma (KS)-one of the most common tumors arising in the setting of immune suppression. Hallmarks of KS lesions include KSHV-infected cells of endothelial lineage and neoangiogenesis. Promigratory factors secreted in the tumor microenvironment by KSHV-infected cells promote endothelial cell (EC) migration and angiogenesis but existing therapies targeting these pathways are not widely utilized. This underscores the need for additional characterization of KSHV-host interactions relevant to EC pathogenesis to identify new therapeutic targets. We recently demonstrated that de novo infection by KSHV promotes EC invasion through upregulation of extracellular matrix metalloproteinase inducer (emmprin)-a multifunctional glycoprotein previously shown to induce tumor cell invasion and regional angiogenesis through upregulation of signal transduction and promotion of tumor-stroma interactions. This study was undertaken to determine whether EC invasion for KSHV-infected cells is induced through activation of specific signal transduction pathways and proangiogenic factors by emmprin. We found that KSHV activation of emmprin induces PI3K/Akt- and mitogen-activated protein kinase (MAPK)-dependent secretion of vascular endothelial growth factor (VEGF). Functionally, EC invasion following de novo infection is induced by emmprin-dependent PI3K/Akt and MAPK activation of VEGF. These findings support the potential utility of targeting emmprin for reducing VEGF secretion and EC migration in the KS microenvironment.

Indexed as

BasiginCell LineEndothelium, VascularEnzyme ActivationEnzyme-Linked Immunosorbent AssayHerpesvirus 8, HumanHumansMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReal-Time Polymerase Chain ReactionRNA InterferenceSignal TransductionUp-RegulationVascular Endothelial Growth Factor ABasiginBSG protein, humanMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor A

Identifiers

PMID21918972
PMCPMC3518925
OpenAlexW2063656743

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.