TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
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Updated: Jul 21, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
Hao Yu1, Kai Zhu1, Minjie Wang1
1Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
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.
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