Zhao Ming-Ming, Wang Bo, Huang Wen-Xi, Zhang Li, Peng Rui, Wang Chao
Department of Gynecology, Obstetrics and Gynecology Hospital, Fudan University Shanghai 200011, China.
School of Basic Medical Sciences, Shanghai Medical College, Fudan University Shanghai 200032, China.
Am J Cancer Res. 2024 Apr 15;14(4):1935-1946. doi: 10.62347/PMYV3832. eCollection 2024.
Endometrial cancer (EC) is a malignancy that poses a threat to woman's health worldwide. Building upon prior work, we explored the inhibitory effect of verteporfin on EC. We showed that verteporfin can damage the mitochondria of EC cells, leading to a decrease of mitochondrial membrane potential and an increase in ROS (reactive oxygen species). In addition, verteporfin treatment was shown to inhibit the proliferation and migration of EC cells, promote apoptosis, and reduce the expression of mitophagy-related proteins PINK1/parkin and TOM20. The ROS inhibitor N-Acetyl Cysteine was able to rescue the expression of PINK1/parkin proteins. This suggests that verteporfin may inhibit mitophagy by elevating ROS levels, thereby inhibiting EC cell viability. The effect of verteporfin on mitophagy supports further investigation as a potential therapeutic option for EC.
子宫内膜癌（EC）是一种在全球范围内对女性健康构成威胁的恶性肿瘤。在先前工作的基础上，我们探究了维替泊芬对子宫内膜癌的抑制作用。我们发现维替泊芬可损伤子宫内膜癌细胞的线粒体，导致线粒体膜电位降低以及活性氧（ROS）增加。此外，维替泊芬处理显示出可抑制子宫内膜癌细胞的增殖和迁移，促进细胞凋亡，并降低线粒体自噬相关蛋白PINK1/帕金和TOM20的表达。活性氧抑制剂N - 乙酰半胱氨酸能够挽救PINK1/帕金蛋白的表达。这表明维替泊芬可能通过提高活性氧水平来抑制线粒体自噬，从而抑制子宫内膜癌细胞的活力。维替泊芬对线粒体自噬的作用支持将其作为子宫内膜癌潜在治疗选择进行进一步研究。
