TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma

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 knoc...

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Bibliographic Details
Published inClinical and translational science Vol. 16; no. 10; pp. 1957 - 1971
Main Authors Yu, Hao, Zhu, Kai, Wang, Minjie, Jiang, Xiaobing
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.10.2023
John Wiley and Sons Inc
Wiley
Subjects
Antibodies
Brain research
Brain tumors
Cell death
Cell viability
Cervical cancer
Ferroptosis
Glioma
Glioma cells
Glutathione
Lipid peroxidation
Lipids
Liver cancer
Medical prognosis
Metastasis
Penicillin
Reactive oxygen species
Regulation
Thioredoxin
Tumors
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Summary: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 Fe 2+ 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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Hao Yu and Kai Zhu contributed equally to this work and share first authorship.
ISSN:1752-8054
1752-8062
1752-8062
DOI:10.1111/cts.13604