Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Cancer Invest. 2011 Jan;29(1):21-8. doi: 10.3109/07357907.2010.535056.
We examined the involvement of peroxiredoxin 6 (Prdx 6) in providing chemoprotection against cisplatin cytotoxicity in SKOV-3 ovarian cancer cells. Treatment of SKOV-3 cells with cisplatin-induced cytotoxicity that was associated with increased accumulation of intracellular reactive oxygen species (ROS) and apoptosis mediated by proteolytically activated caspase 3 and 9. Overexpression of Prdx 6 protein or exposure to N-acetylcysteine (NAC) reversed the apoptotic effect of cisplatin by reducing ROS levels and suppressing the caspase signaling pathway. These results indicate that targeting Prdx 6 may sensitize cancer cells to ROS-producing therapeutic treatments, such as anticancer drugs and radiation.
我们研究了过氧化物酶 6(Prdx 6)在为 SKOV-3 卵巢癌细胞提供顺铂细胞毒性化学保护方面的作用。顺铂处理 SKOV-3 细胞会导致细胞毒性,与细胞内活性氧(ROS)的积累增加以及由蛋白水解激活的 caspase 3 和 9 介导的细胞凋亡有关。Prdx 6 蛋白的过表达或暴露于 N-乙酰半胱氨酸(NAC)通过降低 ROS 水平和抑制半胱氨酸天冬氨酸蛋白酶信号通路来逆转顺铂的凋亡作用。这些结果表明,针对 Prdx 6 可能会使癌细胞对产生 ROS 的治疗方法(如抗癌药物和辐射)敏感。