活性氧诱导的DCTPP1上调促成卵巢癌顺铂耐药。
ROS-Induced DCTPP1 Upregulation Contributes to Cisplatin Resistance in Ovarian Cancer.
作者信息
Wang Yu, Chen Peishi, Chen Xueping, Gong Daoyuan, Wu Yingsong, Huang Liping, Chen Yao
机构信息
Obstetrics and Gynecology Center, Nanfang Hospital, Guangzhou, China.
School of Medical Laboratory and Biotechnology, Southern Medical University, Guangzhou, China.
出版信息
Front Mol Biosci. 2022 Feb 9;9:838006. doi: 10.3389/fmolb.2022.838006. eCollection 2022.
Abstract
Cisplatin resistance hinders the improvement of the prognosis of patients with ovarian cancer. Cisplatin induces cancer cell apoptosis by inducing reactive oxygen species (ROS). dCTP pyrophosphatase 1 (DCTPP1) is a newly discovered dNTP pyrophosphatase. This study aimed to identify the role of DCTPP1 in oxidative stress and cisplatin response of ovarian cancer. Our results indicates cisplatin-induced ROS generation was responsible for the upregulation of DCTPP1 in ovarian cancer cells, whereas DCTPP1 knockdown significantly enhanced the sensitivity of ovarian cancer cells to cisplatin, reflect in reactive oxygen species (ROS) generation, double-strand DNA breaks, and cell apoptosis. The expression of redox-related genes and the activation of the PI3/Akt signaling pathway were also inhibited by DCTPP1 knockdown. Our data proposes that the development of therapeutic approaches targeting DCTPP1 may be useful in the treatment of ovarian cancer.
摘要
顺铂耐药阻碍了卵巢癌患者预后的改善。顺铂通过诱导活性氧（ROS）来诱导癌细胞凋亡。dCTP焦磷酸酶1（DCTPP1）是一种新发现的dNTP焦磷酸酶。本研究旨在确定DCTPP1在卵巢癌氧化应激和顺铂反应中的作用。我们的结果表明，顺铂诱导的ROS生成导致卵巢癌细胞中DCTPP1上调，而敲低DCTPP1显著增强了卵巢癌细胞对顺铂的敏感性，表现为活性氧（ROS）生成、双链DNA断裂和细胞凋亡。敲低DCTPP1还抑制了氧化还原相关基因的表达和PI3/Akt信号通路的激活。我们的数据表明，开发靶向DCTPP1的治疗方法可能对卵巢癌治疗有用。
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