Cooperation between p53 and p73 in cisplatin-induced apoptosis in ovarian carcinoma cells.
The present study was designed to explore the role of p73 in response to cisplatin. In contrast to cisplatin-resistant ovarian carcinoma cells, pharmacological drug concentrations, which caused induction of p53, induced a marginal increase of p73 in sensitive cells. The effect was more marked at high concentrations, with no evidence of p21(WAF1) induction. This behaviour, associated with substantial apoptosis, suggests cell inability to activate DNA damage checkpoint following extensive stress. Although p73 appears to be implicated mainly in response to high stress conditions, the available results support a cooperation between p53 and p73 in cisplatin-induced apoptosis in sensitive cells.
Righetti
Sabina Carla
SC
Fondazione IRCCS Istituto Nazionale Tumori, via Venezian 1, 20133 Milan, Italy.
Perego
Paola
P
Carenini
Nives
N
Zunino
Franco
F
D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002945:Cisplatin / Q000494:pharmacology*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D005260:Female; D006801:Humans; D009687:Nuclear Proteins / Q000378:metabolism*; D010051:Ovarian Neoplasms / Q000473:pathology*; D011485:Protein Binding; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D025521:Tumor Suppressor Proteins / Q000378:metabolism*
D000970:Antineoplastic Agents; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; C000606460:TP73 protein, human; D000072160:Tumor Protein p73; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D002945:Cisplatin