TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma

被引：5

作者：

Yu, Hao ^{[1
]}

Zhu, Kai ^{[1
]}

Wang, Minjie ^{[1
,2
]}

Jiang, Xiaobing ^{[1
,2
]}

机构：

[1] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Neurosurg, Wuhan, Peoples R China

[2] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Neurosurg, Wuhan 430021, Peoples R China

来源：

CTS-CLINICAL AND TRANSLATIONAL SCIENCE | 2023年 / 16卷 / 10期

基金：

中国国家自然科学基金;

关键词：

GLIOBLASTOMA; SURVIVAL; CANCER;

D O I：

10.1111/cts.13604

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Ferroptosis is an iron-dependent cell death process mainly triggered by reactive oxygen species (ROS) and lipid peroxidation. Thioredoxin domain protein 12 (TXNDC12) promotes the development of some tumors; however, its function in tumor ferroptosis remains unclear. In this study, we found that knockdown of TXNDC12 promoted erastin-induced increase in ROS, lipid peroxidation, and Fe2+ levels, and decreased glutathione content. TXNDC12 is involved in ferroptosis by regulating SLC7A11. Further studies showed that TXNDC12 knockdown promoted an erastin-induced decrease in glioma cell viability. Overall, TXNDC12 played a significant role in ferroptosis by modulating SLC7A11 expression. Thus, TXNDC12 and ferroptosis may provide new targets for the treatment of gliomas.

引用

页码：1957 / 1971

页数：15

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