<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">NAIDU, K. AKHILENDER</style></author><author><style face="normal" font="default" size="100%">FANG, QUAN</style></author><author><style face="normal" font="default" size="100%">NAIDU, KAMATHAM A.</style></author><author><style face="normal" font="default" size="100%">CHENG, JIN Q.</style></author><author><style face="normal" font="default" size="100%">NICOSIA, SANTO V.</style></author><author><style face="normal" font="default" size="100%">COPPOLA, DOMENICO</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">p53 Enhances Ascorbyl Stearate-induced G2/M Arrest of Human Ovarian Cancer Cells</style></title><secondary-title><style face="normal" font="default" size="100%">Anticancer Research</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2007</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2007-11-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">3927-3934</style></pages><volume><style face="normal" font="default" size="100%">27</style></volume><issue><style face="normal" font="default" size="100%">6B</style></issue><abstract><style  face="normal" font="default" size="100%">Background: Ascorbyl stearate (Asc-S) is a synthetic ester of ascorbic acid that has been shown to significantly reduce the mutagenic effects of alkylating agents and hepatocarcinogenesis in vivo. We have previously demonstrated that Asc-S inhibits ovarian carcinoma cell proliferation through modulation of the cell cycle. This study was designed to further elucidate the mechanisms underlying such regulation. Materials and Methods: Wild type p53-expressing cell lines (Ov2008 and C13) were used to evaluate the contributions of p53 to Asc-S-induced G2/M arrest. Cell cycle analysis was performed by flow cytometry. Variation of p53, p21, and GADD45 was evaluated by Western blot and RT-PCR. Knockdown of endogenous p53 was achieved by si-RNA. Results: The expression of p53 downstream genes, p21 and GADD45 was upregulated whereas 14-3-3σ was unaffected. Phosphorylation of Cdc2 at residue tyrosine-15 was also induced by Asc-S treatment. However, pSilencer-p53-siRNA only partially rescued the Asc-S induced G2/M arrest. Conclusion: These data show that the anti-proliferative activity of Asc-S on ovarian cancer cells is due in part to G2/M arrest modulated by a p53-dependent pathway. Copyright© 2007 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved</style></abstract></record></records></xml>