Evidence map›Paper›PMID 15342781›Full record

ArticleMolecular biology of the cell2004

Sp1 is involved in Akt-mediated induction of VEGF expression through an HIF-1-independent mechanism.

Nabendu Pore, Shuang Liu, Hui-Kuo Shu, Bin Li, Daphne Haas-Kogan, David Stokoe, Julie Milanini-Mongiat, Gilles Pages, Donald M O'Rourke, Eric Bernhard and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

101 citing papers in PubMed, 226 citations in OpenAlex.

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  13. Review
  14. Sp1 Plays a Key Role in Vasculogenic Mimicry of Human Prostate Cancer Cells.International journal of molecular sciences · 2022
    Article
  15. Review
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41 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 2 countries.

Nabendu PoreDepartment of Radiation Oncology, University of Pennsylvania School of Medicine, Philadelphia, PA 19004, USA.
Shuang Liu
Hui-Kuo Shu
Bin Li
Daphne Haas-Kogan
David Stokoe
Julie Milanini-Mongiat
Gilles Pages
Donald M O'Rourke
Eric Bernhard
Amit Maity
University of Pennsylvania · USInstitut de Recherche sur le Cancer et le Vieillissement de Nice · FRCancer Research Institute · USUniversity of California, San Francisco · US

Funding

SPECIALIZED CENTER OF RESEARCH IN HYPERBARIC OXYGEN THERP50AT000428 · NCCIH · UNIVERSITY OF PENNSYLVANIA · PI THOM, STEPHEN RAYMOND · 2000 to 2004
$7.9M
Regulation of VEGF in Tumors by Ras, EGF and PTENR01CA093638 · NCI · UNIVERSITY OF PENNSYLVANIA · PI MAITY, AMIT · 2002 to 2010
$2.3M
TUMOR RADIOSENSITIZATION BY PRENYLTRANSFERASE INHIBITORSR01CA073820 · NCI · UNIVERSITY OF PENNSYLVANIA · PI BERNHARD, ERIC J · 1998 to 2008
$1.6M
SHP2 and SIRP modulate erbB signals in astrocytesR01CA090586 · NCI · UNIVERSITY OF PENNSYLVANIA · PI O'ROURKE, DONALD M · 2001 to 2005
$1.3M
NCCIH NIH HHS P50 AT000428NCI NIH HHS R01 CA073820NCI NIH HHS R01 CA090586NCI NIH HHS R01 CA093638NCI NIH HHS R01 CA093638-01NCI NIH HHS R01 CA73820-01NCI NIH HHS R01 CA90586-01
6 · The paper itself

Abstract

Increased expression of vascular endothelial growth factor (VEGF) contributes to the growth of many tumors by increasing angiogenesis. Although hypoxia is a potent inducer of VEGF, we previously showed that epidermal growth factor receptor amplification and loss of PTEN, both of which can increase phosphatidylinositol-3-kinase (PI3K) activity, increase VEGF expression. Using both adenoviral vectors and a cell line permanently expressing constitutively active myristoylated Akt (myrAkt), we show that activation of Akt, which is downstream of PI3K, increases VEGF expression in vitro and increases angiogenesis in a Matrigel plug assay. Transient transfection experiments using reporter constructs containing the VEGF promoter showed that up-regulation of VEGF by Akt is mediated through Sp1 binding sites located in the proximal promoter. Small interfering RNA directed against Sp1 prevented the induction of VEGF mRNA in response to myrAkt but not to hypoxia. Expression of myrAkt is associated with increased phosphorylation of Sp1 and its increased binding to a probe corresponding to the -88/-66 promoter region. In conclusion, our results indicate that Sp1 is required for transactivation of the VEGF by Akt. Others have proposed that the PI3K/Akt pathway can increase VEGF expression via the hypoxia-inducible factor 1 (HIF-1); however, our results suggest an alternative mechanism can also operate.

Indexed as

AdenoviridaeAlkaline PhosphataseBase SequenceBinding SitesBlotting, NorthernBlotting, WesternCell LineCell Line, TumorCollagenDensitometryDNA-Binding ProteinsDrug CombinationsGenes, ReporterGreen Fluorescent ProteinsHumansHypoxiaAlkaline PhosphataseCollagenDNA-Binding ProteinsDrug CombinationsGreen Fluorescent ProteinsHIF1A protein, humanHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitLamininmatrigelNuclear ProteinsPhosphatesPhosphatidylinositol 3-KinasesPlicamycinProteoglycansRNA, Small InterferingSp1 Transcription FactorTranscription FactorsVascular Endothelial Growth Factor A

Identifiers

PMID15342781
PMCPMC524732
OpenAlexW2153067410

What OpenQuestion holds

Textmetadata
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.