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Related Experiment Video

Updated: Jul 13, 2026

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

Astrocyte elevated gene-1 activates cell survival pathways through PI3K-Akt signaling.

S-G Lee1, Z-Z Su, L Emdad

  • 1Department of Urology, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, College of Physicians and Surgeons, New York, NY 10032, USA.

Oncogene
|August 21, 2007
PubMed
Summary

Astrocyte elevated gene-1 (AEG-1) acts as an oncogene, promoting cancer by inhibiting apoptosis and activating survival pathways. It cooperates with Ha-ras, a known cancer-driving gene, in tumor development.

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Last Updated: Jul 13, 2026

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

Area of Science:

  • Molecular Biology
  • Oncology
  • Cellular Biology

Background:

  • Astrocyte elevated gene-1 (AEG-1) exhibits oncogenic properties and is upregulated in various cancers.
  • AEG-1 cooperates with the Ha-ras oncogene in promoting cellular transformation and tumorigenesis.
  • Ha-ras oncogene induces AEG-1 expression via the phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway.

Purpose of the Study:

  • To investigate the role of AEG-1 in inducing serum-independent cell growth, a hallmark of oncogenes.
  • To determine if AEG-1 influences apoptosis and survival pathways, particularly in conjunction with Ha-ras.

Main Methods:

  • Overexpression of AEG-1 in cancer cells.
  • Analysis of serum starvation-induced apoptosis and cell growth.
  • Investigation of the PI3K-Akt signaling pathway and its substrates.
  • Measurement of caspase activity.

Main Results:

  • AEG-1 overexpression inhibited serum starvation-induced apoptosis by activating the PI3K-Akt pathway.
  • AEG-1 modulated the phosphorylation of key Akt substrates involved in apoptosis suppression (e.g., GSK3β, c-Myc, MDM2, p53, p21/mda-6, Bad).
  • AEG-1 blocked the activity of caspases activated by serum starvation.

Conclusions:

  • AEG-1 functions as an oncogene that cooperates with Ha-ras and is a downstream target of Ha-ras.
  • AEG-1 plays a significant role in Ha-ras-mediated carcinogenesis, potentially through the activation of cell survival pathways.
  • AEG-1's ability to inhibit apoptosis and promote cell survival contributes to its oncogenic properties.