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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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Detalles Bibliográficos
Autores principales: Yu, Hao, Zhu, Kai, Wang, Minjie, Jiang, Xiaobing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10582671/
https://www.ncbi.nlm.nih.gov/pubmed/37503932
http://dx.doi.org/10.1111/cts.13604
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author Yu, Hao
Zhu, Kai
Wang, Minjie
Jiang, Xiaobing
author_facet Yu, Hao
Zhu, Kai
Wang, Minjie
Jiang, Xiaobing
author_sort Yu, Hao
collection PubMed
description 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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spelling pubmed-105826712023-10-19 TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma Yu, Hao Zhu, Kai Wang, Minjie Jiang, Xiaobing Clin Transl Sci Research 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. John Wiley and Sons Inc. 2023-08-10 /pmc/articles/PMC10582671/ /pubmed/37503932 http://dx.doi.org/10.1111/cts.13604 Text en © 2023 The Authors. Clinical and Translational Science published by Wiley Periodicals LLC on behalf of American Society for Clinical Pharmacology and Therapeutics. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Research
Yu, Hao
Zhu, Kai
Wang, Minjie
Jiang, Xiaobing
TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
title TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
title_full TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
title_fullStr TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
title_full_unstemmed TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
title_short TXNDC12 knockdown promotes ferroptosis by modulating SLC7A11 expression in glioma
title_sort txndc12 knockdown promotes ferroptosis by modulating slc7a11 expression in glioma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10582671/
https://www.ncbi.nlm.nih.gov/pubmed/37503932
http://dx.doi.org/10.1111/cts.13604
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