Evidence map›Paper›PMID 21084864›Full record

ArticleCancer biology & therapy2011

Astrocyte-elevated gene-1 (AEG-1) induction by hypoxia and glucose deprivation in glioblastoma.

Evan Noch, Markus Bookland, Kamel Khalili

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2011. 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
3.4field-weighted citation impact, top 8% 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, 45 citations in OpenAlex.

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  19. Astrocyte elevated gene-1: a novel independent prognostic biomarker for metastatic ovarian tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  20. Astrocyte elevated gene-1 is a novel biomarker of epithelial-mesenchymal transition and progression of hepatocellular carcinoma in two China regions.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Evan NochDepartment of Neuroscience, Center for Neurovirology, Temple University School of Medicine, Philadelphia, PA, USA.
Markus Bookland
Kamel Khalili
Philadelphia University · USTemple College · USTemple University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastomas continue to carry poor prognoses for patients despite advances in surgical, chemotherapeutic, and radiation regimens. One feature of glioblastoma associated with poor prognosis is the degree of hypoxia and expression levels of hypoxia-inducible factor-1 α (HIF-1α). HIF-1α expression allows metabolic adaptation to low oxygen availability, partly through upregulation of VEGF and increased tumor angiogenesis. Here, we demonstrate an induced level of astrocyte-elevated gene-1 (AEG-1) by hypoxia in glioblastoma cells. AEG-1 has the capacity to promote anchorage-independent growth and cooperates with Ha-ras in malignant transformation. In addition, AEG-1 was recently demonstrated to serve as an oncogene and can induce angiogenesis in glioblastoma. Results from in vitro studies show that hypoxic induction of AEG-1 is dependent on HIF-1α stabilization during hypoxia and that PI3K inhibition abrogates AEG-1 induction during hypoxia through loss of HIF-1α stability. Furthermore, we show that AEG-1 is induced by glucose deprivation and that prevention of intracellular reactive oxygen species (ROS) production prevents this induction. Additionally, AEG-1 knockdown results in increased ROS production and increased glucose deprivation-induced cytotoxicity. On the other hand, AEG-1 overexpression prevents ROS production and decreases glucose deprivation-induced cytotoxicity, indicating that AEG-1 induction is necessary for cells to survive this type of cell stress. These observations link AEG-1 overexpression in glioblastoma with hypoxia and glucose deprivation, and targeting these physiological pathways may lead to therapeutic advances in the treatment of glioblastoma in the future.

Indexed as

Cell Adhesion MoleculesCell HypoxiaCell Line, TumorGlioblastomaGlucoseHEK293 CellsHumansHypoxia-Inducible Factor 1Membrane ProteinsRNA-Binding ProteinsRNA, Small InterferingTransfectionCell Adhesion MoleculesGlucoseHypoxia-Inducible Factor 1Membrane ProteinsMTDH protein, humanRNA-Binding ProteinsRNA, Small Interfering

Identifiers

PMID21084864
PMCPMC3047099
OpenAlexW1987792229

What OpenQuestion holds

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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.