ArticleBMC cancer2025
ACSL4 promotes the formation of the proliferative subtype in hepatoblastoma.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- Epigenetic regulation of ACSL4 via H2A monoubiquitylation connects lipid metabolism to BAP1-mediated ferroptosis.Cell death and differentiation · 2026Article
- Reprogramming lipid metabolism in pediatric cancers.Oncogenesis · 2026Review
- Long-chain acyl-CoA synthetases: biological functions, diseases and therapeutic targets.Molecular biomedicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Hepatoblastoma (HB) is the most common pediatric liver malignancy, with its significant heterogeneity complicating the identification of the most aggressive subtypes and the development of targeted therapies. In this study, we performed transcriptomic analysis of HB samples from the GEO database and identified three distinct molecular subtypes with varying prognostic outcomes. Among them, the proliferative subtype, characterized by enhanced proliferative capacity, poor prognosis, and an immunosuppressive tumor microenvironment, was particularly notable. ACSL4 emerged as a critical biomarker of this proliferative subtype, driving HB cell proliferation both in vitro and in vivo. Furthermore, pharmacological inhibition of ACSL4 using abemaciclib significantly suppressed tumor growth in xenograft models. Mechanistically, ACSL4 was found to promote cell proliferation by downregulating the interferon response signaling pathway which may implicate contribution to immunosuppression in the tumor. These findings underscore the pivotal role of ACSL4 in HB progression and highlight its potential as a therapeutic target for aggressive HB subtypes.
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Registered trials
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