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Peroxiredoxin I and II as novel therapeutic molecular targets in cervical cancer treatment through regulation of endoplasmic reticulum stress induced by bleomycin
Cell Death Discovery ( IF 6.1 ) Pub Date : 2024-05-31 , DOI: 10.1038/s41420-024-02039-7
Hu-Nan Sun 1 , Da-Yu Ma 1 , Xiao-Yu Guo 1 , Ying-Ying Hao 1 , Mei-Hua Jin 1 , Ying-Hao Han 1 , Xun Jin 2 , Taeho Kwon 3, 4
Affiliation  

Cervical cancer, significantly affecting women worldwide, often involves treatment with bleomycin, an anticancer agent targeting breast, ovarian, and cervical cancers by generating reactive oxygen species (ROS) to induce cancer cell death. The Peroxiredoxin (PRDX) family, particularly PRDX1 and 2, plays a vital role in maintaining cellular balance by scavenging ROS, thus mitigating the damaging effects of bleomycin-induced mitochondrial and cellular oxidative stress. This process reduces endoplasmic reticulum (ER) stress and prevents cell apoptosis. However, reducing PRDX1 and 2 levels reverses their protective effect, increasing apoptosis. This research highlights the importance of PRDX1 and 2 in cervical cancer treatments with bleomycin, showing their potential to enhance treatment efficacy by managing ROS and ER stress and suggesting a therapeutic strategy for improving outcomes in cervical cancer treatment.



中文翻译:


过氧化还原蛋白 I 和 II 通过调节博来霉素诱导的内质网应激作为宫颈癌治疗的新治疗分子靶点



宫颈癌对全世界女性都有重大影响,通常需要使用博莱霉素进行治疗,博莱霉素是一种针对乳腺癌、卵巢癌和宫颈癌的抗癌剂,通过产生活性氧 (ROS) 诱导癌细胞死亡。过氧化氧还蛋白 (PRDX) 家族,特别是 PRDX1 和 2,通过清除 ROS 在维持细胞平衡中发挥着至关重要的作用,从而减轻博来霉素诱导的线粒体和细胞氧化应激的破坏作用。这一过程可减少内质网 (ER) 应激并防止细胞凋亡。然而,降低 PRDX1 和 2 水平会逆转它们的保护作用,增加细胞凋亡。这项研究强调了 PRDX1 和 2 在博莱霉素宫颈癌治疗中的重要性,显示了它们通过管理 ROS 和 ER 应激来提高治疗效果的潜力,并提出了改善宫颈癌治疗结果的治疗策略。

更新日期:2024-05-31
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