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Updated: Jun 24, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Switching Akt: from survival signaling to deadly response

Marek Los1, Subbareddy Maddika, Bettina Erb

  • 1Interfaculty Institute for Biochemistry, University of Tübingen, Tübingen, Germany.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|March 26, 2009
PubMed

Insights

The protein kinase Akt, often overactive in tumors, can surprisingly promote cancer cell death. This occurs by Akt increasing reactive oxygen species and reducing antioxidant defenses, creating a vulnerability for targeted therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Akt protein kinase is frequently hyperactivated in various tumors.
  • Akt plays a critical role in cancer cell survival and therapeutic resistance.
  • Evidence suggests Akt may have a dual role in cell death regulation.

Purpose of the Study:

  • To investigate the previously unrecognized function of Akt in promoting cell death.
  • To elucidate the mechanisms by which Akt influences cell death pathways.
  • To identify potential therapeutic strategies targeting Akt-driven tumor vulnerabilities.

Main Methods:

  • Analysis of Akt's role in cell survival and death pathways.
  • Investigation of Akt's impact on reactive oxygen species (ROS) production.
  • Assessment of Akt's regulation of antioxidant enzyme expression and activity.

Main Results:

  • Akt is not solely a pro-survival kinase; it can facilitate cell death under specific conditions.
  • Akt increases intracellular reactive oxygen species levels.
  • Akt suppresses the activity and expression of key antioxidant enzymes.

Conclusions:

  • Akt's ability to down-regulate antioxidant defenses represents a novel therapeutic target.
  • Targeting Akt-mediated suppression of antioxidant defenses could lead to selective tumor cell eradication.
  • Oxidant therapies may be effective against tumors with high Akt activity by exploiting this Achilles' heel.

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