ArticleThe Journal of clinical investigation2024
VHL governs m6A modification and PIK3R3 mRNA stability in clear cell renal cell carcinomas.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- ELABELA targets the METTL3/PI3K/AKT axis to enhance trophoblast invasion in early-onset preeclampsia.BMC pregnancy and childbirth · 2026Article
- RNA methylation in urological cancers: regulatory logic, biological functions, and clinical relevance.Frontiers in immunology · 2026Review
- A SWI/SNF complex-related genes signature predicts prognosis and immune infiltration in ccRCC with KCNK5 as a novel biomarker.Scientific reports · 2025Article
- Hypoxia-mediated regulation of mRNA metabolism: from transcription to stability.Cell communication and signaling : CCS · 2025Review
- Decoding mJournal of translational medicine · 2025Review
- METTL Family in Healthy and Disease.Molecular biomedicine · 2024Review
- N6-methyladenosine modification of hypoxia-inducible factor-1α regulatesWorld journal of gastrointestinal oncology · 2024Article
- Critical role of non-coding RNA-mediated ferroptosis in urologic malignancies.Frontiers in immunology · 2024Review
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3 authors at 2 institutions in 1 country.
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Abstract
N6-Methyladenosine (m6A), a prevalent posttranscriptional modification, plays an important role in cancer progression. Clear cell renal cell carcinoma (ccRCC) is chiefly associated with the loss of the von Hippel-Lindau (VHL) gene, encoding a component of the E3 ubiquitin ligase complex. In this issue of the JCI, Zhang and colleagues unveiled a function of VHL beyond its canonical role as an E3 ubiquitin ligase in regulating hypoxia-inducible factors (HIFs). It also governed m6A modification by orchestrating the assembly of m6A writer proteins METTL3 and METTL14, thereby stabilizing PIK3R3 mRNA. Mechanistically, PIK3R3 contributed to p85 ubiquitination, which restrained PI3K/AKT signaling and consequently impeded ccRCC growth in cell and mouse models. This discovery provides potential treatment targets in VHL-deficient ccRCCs.
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