ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
LEDGF Binds H3R17me2a Promoting De Novo Nucleotide Biosynthesis in SETD2 Mutant Clear Cell Renal Cell Carcinoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- AI-guided discovery of the IRF4-PAICS-LDHA axis as a multitarget hub linking tumor metabolism to CD8+ T cell exhaustion in DLBCL.NPJ precision oncology · 2026Article
- Emerging roles for the epigenetic modifiers PBRM1 SETD2 and BAP1 in clear cell renal cell carcinoma pathogenesis and prognosis beyond VHL.Discover oncology · 2026Review
- Integrative analysis of scRNA-seq and bulk RNA-seq with machine learning develops a nucleotide metabolism-based prognostic model for ccRCC and reveals the function of IFI30.Frontiers in oncology · 2026Article
- LEDGF Binds H3R17me2a Promoting De Novo Nucleotide Biosynthesis in SETD2 Mutant Clear Cell Renal Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
12 authors.
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Abstract
Previous studies have identified that lens epithelium-derived growth factor (LEDGF) interacts with SETD2-dependent histone H3 trimethylated at lysine 36 (H3K36me3) to mediate transcriptional elongation. However, the original LEDGF recognition H3K36me3 epigenetic regulatory axis no longer exists in SETD2 mutant clear cell renal cell carcinoma (ccRCC) patients, and a new transcription system needs to be discovered. In this study, the authors demonstrated the novel interaction between LEDGF and H3R17me2a. In detail, Asn38 and Asp57 of LEDGF Proline-Tryptophan-Tryptophan-Proline (PWWP) domain are the key binding sites validated by peptide pull-down assays. Subsequently, a series of in vitro and in vivo experiments showed that PPAT, PAICS, GART, ADSL, and ADSS2 are key target genes. Collectively, LEDGF binds H3R17me2a to regulate purine nucleotide metabolism in SETD2 mutant ccRCC cells, promoting tumor proliferation, and may be an effective therapeutic target.
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