Chung Y M, Yoo Y D, Park J K, Kim Y T, Kim H J
Laboratory of Experimental Therapeutics, Korea Cancer Center Hospital, Seoul 139-706, Korea.
Anticancer Res. 2001 Mar-Apr;21(2A):1129-33.
Peroxiredoxin II (Prx II) has been known to be induced by various oxidative stimuli and to play an important protective role from oxidative damage by hydrogen peroxide (H2O2). In this study, we observed that cisplatin as well as H2O2 induced Prx II expression. To examine the correlation between the increased expression of Prx II and chemoresistance, we prepared a Prx II-overexpressing cell line, SNU638 cells, and found it to be more resistant to cell death induced by cisplatin and H2O2 than neo-transfectant cells. We also observed that enhanced expression of Prx II inhibited cisplatin- and H2O2-induced apoptosis, demonstrating that resistance to these cytotoxic agents was due to inhibition of apoptosis. The above results led us to suggest that the overexpressed Prx II protein inhibits cisplatin-induced apoptosis, thereby contributing to chemoresistance of tumor cells, especially to oxidative stress producing anticancer drugs.
过氧化物酶II（Prx II）已知可被各种氧化刺激诱导，并在抵御过氧化氢（H2O2）的氧化损伤中发挥重要的保护作用。在本研究中，我们观察到顺铂以及H2O2均可诱导Prx II表达。为了研究Prx II表达增加与化疗耐药性之间的相关性，我们制备了过表达Prx II的细胞系SNU638细胞，并发现其比新转染细胞对顺铂和H2O2诱导的细胞死亡更具抗性。我们还观察到Prx II的表达增强可抑制顺铂和H2O2诱导的细胞凋亡，这表明对这些细胞毒性药物的抗性是由于细胞凋亡受到抑制。上述结果使我们推测，过表达的Prx II蛋白可抑制顺铂诱导的细胞凋亡，从而导致肿瘤细胞产生化疗耐药性，尤其是对产生氧化应激的抗癌药物耐药。
