Objective： To analyze the gene structure and characteristics of ferredoxin 1 (FDX1), a key regulatory gene for cuproptosis, using bioinformatics methods. Methods： The human FDX1 DNA sequence was obtained from GenBank database, and bioinformatics analysis of FDX1 general characteristics, structural recognition, characteristic analysis, and tissue expression was conducted by using data mining software. Results： The human FDX1 gene is located at 11q22.3, with a total length of 35 553 bp, strong codon bias, and the repetitive sequence accounting for 61.40% of the total length of the gene. There are 5 promoters (score>0.90), 71 transcription factor binding sites and polyadenylation tail signal at site 518 in the upstream 2 000 bp region, and no CpG island can be predicted. Subcellular localization of FDX1 is most likely in the mitochondria. The molecular function prediction showed that FDX1 had 2Fe-2S cluster binding activity. The maximum mRNA of human FDX1 gene expression was in the adrenal gland ［146(100×FPKM)1/2］. The cancer specificity of FDX1 mRNA in each tissue is low. Conclusion： The mitochondrial subcellular localization, 2Fe-2S cluster activity, and involved signaling pathways of FDX1 have been confirmed that FDX1 could be used as a key regulatory genes for cuproptosis from the perspective of biological algorithms.

铜是几乎所有生物体必需的一种金属元素，在生命活动中起重要的调节作用。调节性细胞死亡(regulatory cell death,RCD)包含多种细胞死亡方式，如铁死亡、焦亡、坏死性凋亡等且多与铜代谢相关。近期，研究发现一种新型的铜依赖性RCD，并命名为“铜死亡(cuproptosis)”，即铜离子通过促进三羧酸循环中的脂酰化修饰蛋白聚集，使细胞产生毒性应激从而导致细胞死亡。本文针对铜稳态及铜依赖性细胞死亡调控机制在消化系统肿瘤中的研究进展作一综述。