ArticleJHEP reports : innovation in hepatology2025
FKBP9 enhances IGF2BP1-mediated m
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- PRMT3 in cancer: arginine methylation as a driver of tumor metabolism, immune evasion, and therapeutic resistance.Frontiers in immunology · 2026Review
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background & Aims: N Methods: The expression of FKBP9 in HCC was profiled by reverse-transcription quantitative PCR, western blot, ELISA, and immunohistochemistry. Cell proliferation, migration, invasion, apoptosis, and mRNA stability were examined using CCK-8, colony formation, flow cytometry, and cycloheximide treatment. An orthotopic allograft tumor model was constructed for Results: FKBP9 was significantly upregulated in both HCC tissues and serum ( Conclusions: FKBP9 promotes HCC progression by facilitating IGF2BP1 recognition of m6A-modified transcripts, thereby stabilizing MYC and PDGFB. The FKBP9-IGF2BP1 axis represents a potential therapeutic target in HCC. Impact and implications: This study highlights the critical role of FKBP9 in hepatocellular carcinoma progression by regulating IGF2BP1-mediated m6A RNA recognition, thereby enhancing the stability of key oncogenic transcripts such as
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Registered trials
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