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TAp73alpha protects small cell lung carcinoma cells from caspase-2 induced mitochondrial mediated apoptotic cell

Naveen Muppani1, Ulrika Nyman, Bertrand Joseph

  • 1Department of Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, 171 76 Stockholm, Sweden.

Oncotarget
|December 29, 2011
PubMed

Insights

The TAp73alpha protein inhibits caspase-2 activity, preventing apoptosis and promoting tumor growth. This finding highlights TAp73alpha

Area of Science:

  • Molecular Biology
  • Cell Death Pathways
  • Cancer Biology

Background:

  • Caspase-2 is a highly conserved mammalian caspase activated by death stimuli, preceding mitochondrial dysfunction and apoptosis.
  • Caspase-2 exhibits tumor suppressor functions in vivo.
  • The TAp73alpha isoform, upregulated in tumors, can repress drug-induced apoptosis in a cell-type specific manner.

Purpose of the Study:

  • To investigate the interaction between TAp73alpha and caspase-2.
  • To determine how TAp73alpha influences caspase-2 activity and downstream apoptotic events.
  • To elucidate the role of TAp73alpha in modulating caspase-2-mediated cell death.

Main Methods:

  • Assessed the effect of TAp73alpha on caspase-2 enzymatic activity.
  • Quantified caspase-2-induced Bax activation and mitochondrial membrane potential loss.
  • Investigated the structural domains of TAp73alpha required for caspase-2 inhibition.

Main Results:

  • TAp73alpha directly represses caspase-2 enzymatic activity.
  • This repression by TAp73alpha reduces caspase-2-mediated Bax activation and mitochondrial dysfunction.
  • The inhibitory effect of TAp73alpha on caspase-2 requires its DNA binding and SAM domains.

Conclusions:

  • TAp73alpha acts as an inhibitor of caspase-2-induced apoptosis.
  • The oncogenic potential of TAp73alpha is strengthened by its ability to inhibit caspase-2, especially given its upregulation in certain tumors.

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