Li Yanhu, Zhang Haijun, Yang Fengguang, Zhu Daxue, Chen Shijie, Wang Zhaoheng, Wei Ziyan, Yang Zhili, Jia Jingwen, Zhang Yizhi, Wang Dongxin, Ma Mingdong, Kang Xuewen
Lanzhou University Second Hospital, Lanzhou, PR China.
Orthopaedics Key Laboratory of Gansu Province, Lanzhou, PR China.
Cell Prolif. 2025 Jan;58(1):e13752. doi: 10.1111/cpr.13752. Epub 2024 Oct 1.
SLC7A11 plays a pivotal role in tumour development by facilitating cystine import to enhance glutathione synthesis and counteract oxidative stress. Disulphidptosis, an emerging form of cell death observed in cells with high expression of SLC7A11 under glucose deprivation, is regulated through reduction-oxidation reactions and disulphide bond formation. This process leads to contraction and collapse of the F-actin cytoskeleton from the plasma membrane, ultimately resulting in cellular demise. Compared to other forms of cell death, disulphidptosis exhibits distinctive characteristics and regulatory mechanisms. This mechanism provides novel insights and innovative strategies for cancer treatment while also inspiring potential therapeutic approaches for other diseases. Our review focuses on elucidating the molecular mechanism underlying disulphidptosis and its connection with the actin cytoskeleton, identifying alternative metabolic forms of cell death, as well as offering insights into disulphidptosis-based cancer therapy. A comprehensive understanding of disulphidptosis will contribute to our knowledge about fundamental cellular homeostasis and facilitate the development of groundbreaking therapies for disease treatment.
溶质载体家族7成员11（SLC7A11）通过促进胱氨酸的摄取以增强谷胱甘肽的合成并对抗氧化应激，在肿瘤发展中起关键作用。二硫化物诱导的细胞死亡是在葡萄糖剥夺条件下，在高表达SLC7A11的细胞中观察到的一种新出现的细胞死亡形式，其通过氧化还原反应和二硫键形成进行调节。这个过程导致F-肌动蛋白细胞骨架从质膜收缩和塌陷，最终导致细胞死亡。与其他形式的细胞死亡相比，二硫化物诱导的细胞死亡表现出独特的特征和调节机制。这一机制为癌症治疗提供了新的见解和创新策略，同时也启发了其他疾病的潜在治疗方法。我们的综述着重于阐明二硫化物诱导的细胞死亡的分子机制及其与肌动蛋白细胞骨架的联系，确定细胞死亡的替代代谢形式，并提供基于二硫化物诱导的细胞死亡的癌症治疗见解。全面了解二硫化物诱导的细胞死亡将有助于我们对基本细胞稳态的认识，并促进疾病治疗的突破性疗法的发展。
