ArticleFrontiers in oncology2025
Dual oncogenic role of RNF220 in AML: linking metabolic rewiring to cell proliferation and immune evasion.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- MO-IPS suppresses acute myeloid leukemia through metabolic reprogramming and synergizes with anti-PD-1 immunotherapy.Functional & integrative genomics · 2026Article
- Decoding coronary artery calcification: metabolic reprogramming features and a promising circulating biomarker PXDN.Frontiers in cell and developmental biology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Background: Acute myeloid leukemia (AML) remains a clinical challenge with suboptimal long-term survival. While circular RNAs derived from the RNF220 host gene have been implicated in AML pathogenesis, the functional role and regulatory mechanisms of RNF220 itself in AML are poorly understood. Methods: We integrated bioinformatics analyses of public databases (TCGA-LAML, TARGET-LAML) and local cohort with Results: RNF220 overexpression correlated with poor prognosis in AML, drove an immunosuppressive microenvironment characterized by reduced CD8 Conclusion: NF220 acts as an oncogenic ubiquitin ligase in AML by coordinating dual pro-leukemic mechanisms: cell-intrinsic metabolic rewiring (glycolysis/phenylalanine) and immune evasion via microenvironment suppression. Targeting the FOXA1-RNF220 axis may offer novel therapeutic strategies for high-risk AML.
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