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The tumor suppressor Caliban regulates DNA damage-induced apoptosis through p53-dependent and -independent activity

Y Wang1, Z Wang, B H Joshi

  • 1CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, China.

Oncogene
|September 12, 2012
PubMed

Insights

Caliban (Clbn) regulates DNA damage-induced apoptosis through p53-dependent and -independent pathways. This tumor suppressor function was confirmed in non-small-cell lung cancer cells and in vivo.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Caliban (Clbn) is the Drosophila homolog of the human Serologically defined colon cancer antigen 1 gene.
  • Previous studies indicated Clbn's tumor suppressor role in non-small-cell lung cancer (NSCLC) cells, but its mechanism was unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying Caliban's tumor suppressor function.
  • To investigate the role of Clbn in DNA damage response and apoptosis.

Main Methods:

  • Generated clbn knockout flies using homologous recombination.
  • Assessed sensitivity to irradiation in wild-type and knockout flies.
  • Analyzed apoptosis pathways, including p53-dependent and -independent mechanisms, caspase activity, and the proapoptotic gene Hid.
  • Evaluated the effect of ectopic clbn expression in NSCLC cells in an athymic nude mouse model.

Main Results:

  • Clbn knockout flies exhibited heightened sensitivity to irradiation.
  • Normal Clbn function is essential for both p53-dependent and -independent DNA damage-induced apoptosis.
  • Clbn demonstrated a two-stage upregulation following DNA damage, coordinating different apoptosis pathways.
  • Clbn possesses proapoptotic functions, interacting with caspase and the Hid gene.
  • Ectopic expression of clbn suppressed tumor formation in NSCLC cells xenografted into mice.

Conclusions:

  • Caliban acts as a crucial regulator of DNA damage-induced apoptosis.
  • Clbn functions as a tumor suppressor by modulating both p53-dependent and -independent apoptotic pathways.
  • These findings highlight Caliban's potential as a therapeutic target in NSCLC and other cancers.

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