ArticleGenes and immunity2023
Integrated analyses reveal the prognostic, immunological features and mechanisms of cuproptosis critical mediator gene FDX1 in KIRC.
Article in Genes and immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Integrative omics profiling of CRELD2 in ccRCC: a nexus of genetics, prognosis, and tumor microenvironment.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Role of Ferredoxin 1Cancer pathogenesis and therapy · 2026Review
- The molecular mechanism and therapeutic landscape of copper and cuproptosis in cancer.Signal transduction and targeted therapy · 2025Review
- Unveiling ammonia-induced cell death: a new frontier in clear cell renal cell carcinoma prognosis.Frontiers in immunology · 2025Article
- Cuproptosis in cancer: biological implications and therapeutic opportunities.Cellular & molecular biology letters · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ferredoxin 1 (FDX1) gene had been recently reported as a critical mediator of cuproptosis, and without doubt, its roles in KIRC would be of importance. Hence, this paper was to explore the roles of FDX1 in kidney renal clear cell carcinoma (KIRC) and its potential molecular mechanisms via scRNA-sequencing and bulk RNA-sequencing analyses. FDX1 was lowly expressed in KIRC and validated both at the protein and mRNA levels (all p < 0.05). Moreover, its elevated expression was linked with a better overall survival (OS) prognosis in KIRC (p < 0.01). The independent impact of FDX1 on KIRC prognosis was demonstrated by univariate/multivariate regression analysis (p < 0.01). Gene set enrichment analysis (GSEA) identified seven pathways strongly associated with FDX1 in KIRC. Furthermore, FDX1 was also revealed to be significantly related with immunity (p < 0.05). In addition, patients with low expression of FDX1 might be more sensitive to immunotherapies. ScRNA-seq analysis found that FDX1 could be expressed in immune cells and was mainly differently expressed in Mono/Macro cells. Ultimately, we also identified several LncRNA/RBP/FDX1 mRNA networks to reveal its underlying mechanisms in KIRC. Taken together, FDX1 was closely related to prognosis and immunity in KIRC, and its RBP-involved mechanisms of LncRNA/RBP/FDX1 networks were also revealed by us.
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