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Akt1 and dCIZ1 promote cell survival from apoptotic caspase activation during regeneration and oncogenic overgrowth

Gongping Sun1,2, Xun Austin Ding3, Yewubdar Argaw3

  • 1The Key Laboratory of Experimental Teratology, Ministry of Education and Department of Anatomy and Histoembryology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China. sgp@sdu.edu.cn.

Nature Communications
|November 13, 2020
PubMed

Insights

Some cells can survive apoptosis, a programmed cell death. This survival aids tissue repair in Drosophila and is co-opted by oncogenes, driving tumor growth.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Apoptosis, or programmed cell death, is a fundamental biological process.
  • Executioner caspase activation during apoptosis was historically viewed as irreversible.
  • Recent findings suggest cells can survive caspase activation, prompting investigation into its mechanisms and significance.

Purpose of the Study:

  • To investigate the physiological role of cell survival after executioner caspase activation.
  • To identify molecular factors enabling survival from apoptosis.
  • To explore the connection between this survival mechanism and oncogene-induced proliferation.

Main Methods:

  • Utilized Drosophila wing disc model for studying tissue injury and regeneration.
  • Performed RNA interference (RNAi) screening to identify survival genes.
  • Investigated the role of identified genes (akt1, CG8108/dCIZ1) in survival and overgrowth.

Main Results:

  • Drosophila wing disc cells surviving executioner caspase activation contribute to tissue regeneration after injury.
  • Akt1 and the Drosophila CIZ1 homolog (dCIZ1) are essential for surviving caspase activation.
  • Activated oncogenes induce caspase activation, and Akt1/dCIZ1 are required for their survival and subsequent overgrowth.

Conclusions:

  • Survival following executioner caspase activation is a natural tissue repair mechanism.
  • This survival pathway is hijacked during oncogene-driven tumorigenesis.
  • Akt1 and dCIZ1 play critical roles in both tissue regeneration and cancer progression.

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