Gaoxiang Chen, Jianan Zhang, Weifeng Teng, Yong Luo, Xiaochun Ji
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引用次数: 0
Abstract
Cuprotosis is a recently identified cell death form that caused by intracellular copper accumulation and regulated by FDX1. This work aimed to explore the role of cuprotosis and the pivotal regulatory gene FDX1 in thyroid cancer development. We observed that expression of FDX1 in tumor section was notably lower than that in non-tumor sections in clinical samples. Induction of cuprotosis by elesclomol (ES) significantly repressed the in vitro and in vivo growth of thyroid cancer cells, simultaneously elevated Cu level and expression of FDX1, whereas depletion of FDX1 abolished these effects. Knockdown of FDX1 decreased the lipoylation level of DLAT and DLST in thyroid cancer cells, alleviated cuprotosis-induced cell death, simultaneously upregulated the levels of PA and α-KG. These findings demonstrated that FDX1 promotes the cuprotosis of thyroid cancer cells via regulating the lipoylation of DLAT.
期刊介绍:
Heliyon is an all-science, open access journal that is part of the Cell Press family. Any paper reporting scientifically accurate and valuable research, which adheres to accepted ethical and scientific publishing standards, will be considered for publication. Our growing team of dedicated section editors, along with our in-house team, handle your paper and manage the publication process end-to-end, giving your research the editorial support it deserves.