ArticleCellular and molecular life sciences : CMLS2026
TRIM21-Mediated ubiquitination of FBL suppresses PI3K/AKT signaling and tumor progression in clear cell renal cell carcinoma.
Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundClear cell renal cell carcinoma (ccRCC) frequently exhibits transcriptional reprogramming driven by oncogenic C-Myc. Fibrillarin (FBL), a nucleolar C-Myc target, is markedly upregulated in ccRCC, correlating with poor prognosis and essential for tumor cell survival.
methodsIntegrated single-cell RNA sequencing, bulk transcriptomics, and proteomics were used to identify FBL as a key target. Functional assays, immunoprecipitation-mass spectrometry, and molecular docking were performed to investigate FBL's oncogenic mechanisms and interaction with TRIM21.
resultsFBL promotes ccRCC cell proliferation, migration, and tumor growth via PI3K/AKT pathway activation. TRIM21 was identified as a novel FBL-binding E3 ubiquitin ligase that catalyzes K48-linked polyubiquitination of FBL at lysine 292, accelerating its proteasomal degradation. TRIM21 overexpression reduces FBL levels, inhibits PI3K/AKT signaling, and reverses FBL-induced oncogenic phenotypes. TRIM21 is downregulated in ccRCC tissues and associated with unfavorable prognosis.
conclusionsThe TRIM21-FBL axis regulates ccRCC progression by modulating PI3K/AKT signaling, providing mechanistic insight and potential therapeutic targets for ribosome biogenesis and oncogenic signaling.
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