Activation of p53-dependent responses in tumor cells treated with a PARC-interacting peptide.

We tested the activity of a p53 carboxy-terminal peptide containing the PARC-interacting region in cancer cells with wild type cytoplasmic p53. Peptide delivery was achieved by fusing it to the TAT transduction domain (TAT-p53-C-ter peptide). In a two-hybrid assay, the tetramerization domain (TD) of p53 was necessary and sufficient to ...
bind PARC. The TAT-p53-C-ter peptide disrupted the PARC-p53 complex. Peptide treatment caused p53 nuclear relocation, p53-dependent changes in gene expression and enhancement of etoposide-induced apoptosis. These studies suggest that PARC-interacting peptides are promising candidates for the enhancement of p53-dependent apoptosis in tumors with wt cytoplasmic p53.
Mesh Terms:
Apoptosis, Cell Line, Tumor, DNA Topoisomerase IV, Humans, Neoplasms, Signal Transduction, Tumor Suppressor Protein p53
Biochem. Biophys. Res. Commun.
Date: Apr. 04, 2008
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