ArticleJournal of cancer research and clinical oncology2025
FBXW11 inhibits tumorigenesis by ubiquitinating YB1 in hepatocarcinoma.
Article in Journal of cancer research and clinical 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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2 citing papers in PubMed.
- LIN-23 AffectsbioRxiv : the preprint server for biology · 2026Article
- YBX1 as an adaptive RNA hub in cancer: linking state-dependent RNA regulation to tumor immunity, metabolic reprogramming, and therapy resistance.Frontiers in immunology · 2026Review
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6 authors.
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Abstract
purposeThe study aimed to investigate the role of FBXW11 in hepatocellular carcinoma (HCC) and its underlying mechanism. Specifically, we explored whether FBXW11 inhibits tumorigenesis by regulating YB1 ubiquitination and elucidated the functional significance of the FBXW11-YB1 axis in HCC progression.
methodsClinical HCC specimens and cell lines (HCC-LM3, HuH7, Hep3B, SNU-449) were used. FBXW11 and YB1 expression were analyzed via Western blotting and immunohistochemistry (IHC). Gain- and loss-of-function assays (FBXW11 overexpression/knockdown) were performed to assess cell proliferation. Co-immunoprecipitation (Co-IP), mass spectrometry, and ubiquitination assays identified protein interactions and ubiquitination patterns. In vivo tumorigenesis was evaluated using xenograft models in nude mice. Correlations with clinicopathological features and survival were analyzed via statistical methods.
resultsFBXW11 was significantly downregulated in HCC tissues, correlated with advanced TNM stages and poor overall survival (HR = 3.058, P = 0.042). FBXW11 overexpression suppressed HCC cell proliferation, while knockdown enhanced it. Mechanistically, FBXW11 directly interacted with the cold shock domain (CSD) of YB1, promoting K48-linked polyubiquitination and proteasomal degradation of YB1. YB1 overexpression rescued the tumor-suppressive effects of FBXW11 overexpression. In vivo, FBXW11 overexpression inhibited tumor growth by suppressing the YB1/Akt/mTOR signaling pathway, which was rescued by YB1 re-expression.
conclusionFBXW11 acts as a tumor suppressor in HCC by mediating YB1 ubiquitination and degradation, thereby inhibiting the Akt/mTOR pathway. The FBXW11-YB1 axis represents a novel regulatory mechanism in hepatocarcinogenesis, highlighting FBXW11 as a potential prognostic biomarker and therapeutic target for HCC.
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