Abstract
Inactivation of the p53 tumor suppressor protein has been observed in a large number of human cancers. Overexpression of p53 induces either growth arrest or programmed cell death (apoptosis). The growth arrest function of p53 is mediated by induction of p21 (WAF1/CIP1), but the mechanisms underlying p53-dependent apoptosis are still largely unknown. To investigate these mechanisms, we have identified six differentially expressed transcripts in a human colon cancer cell line undergoing p53 dependent apoptosis. One of the p53-responsive genes showed significant homology to Drosophila peroxidasin, an extracellular matrix-associated peroxidase, and is likely to be its human homologue. Our results suggest a possible connection between p53-dependent apoptosis and the production of reactive oxygen species.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 864-869 |
| Number of pages | 6 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 261 |
| Issue number | 3 |
| DOIs | |
| State | Published - Aug 11 1999 |
Funding
We thank P. Shaw for EB and EB1 cell lines. We also thank T. Nagase for the cDNA clone. This work was supported by a grant from the National Cancer Institute (CA41086). T. S. is an Investigator of the Howard Hughes Medical Institute and an American Cancer Society Professor.
ASJC Scopus subject areas
- Molecular Biology
- Biophysics
- Biochemistry
- Cell Biology
