GPX4
程序性细胞死亡
细胞凋亡
促炎细胞因子
自噬
细胞生物学
癌细胞
诱导剂
化学
癌症
癌症研究
活性氧
一氧化碳
生物
生物化学
炎症
免疫学
氧化应激
基因
谷胱甘肽过氧化物酶
过氧化氢酶
催化作用
遗传学
作者
Wei Cao,Mingyu Sun,K.N. Yu,Lele Zhao,Feng Yang,Chunyan Tan,Miaomiao Yang,Ying Wang,Feng-qin Zhu,Lianjun Chen,Lili Nie,Ye Zhao,Guodong Chen,Wei Han
标识
DOI:10.1038/s41420-023-01743-0
摘要
Abstract The gas therapy is drawing increasing attention in the treatment of many diseases including cancer. As one of gas signaling molecules, carbon monoxide (CO) has been proved to exert anti-cancer effects via triggering multiple cell death types, such as autophagy, apoptosis and necrosis. Here, we showed that low concentration CO delivered from CO-releasing molecule 3 (CORM-3) effectively induced ferroptosis, known as a novel proinflammatory programmed cell death, in vitro and in vivo. Mechanistically, we found that CO triggered ferroptosis by modulating the ROS/GSK3β/GPX4 signaling pathway, resulting in the accumulation of lipid hydroperoxides and the occurrence of ferroptosis. We think our findings provide novel insights into the anti-cancer mechanisms of CO, and suggest that CO could potentially be exploited as a novel ferroptosis inducer for cancer treatment in the future.
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