TY - JOUR
T1 - Isolation of differentially expressed cDNAs from p53-dependent apoptotic cells
T2 - Activation of the human homologue of the Drosophila peroxidasin gene
AU - Horikoshi, Nobuo
AU - Cong, Jainping
AU - Kley, Nikoli
AU - Shenk, Thomas
N1 - Funding Information:
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.
PY - 1999/8/11
Y1 - 1999/8/11
N2 - 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.
AB - 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.
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U2 - 10.1006/bbrc.1999.1123
DO - 10.1006/bbrc.1999.1123
M3 - Article
C2 - 10441517
AN - SCOPUS:0033546727
SN - 0006-291X
VL - 261
SP - 864
EP - 869
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -