ArticleJournal of translational medicine2025
LncRNA938/ TAF9/TTK axis promotes EMT and serves as a therapeutic target in hepatoblastoma.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
Abstract
backgroundHepatoblastoma (HB) is the most common malignant liver tumor in children. The expression of TAF9 is frequently upregulated in HB; however, its underlying molecular mechanisms are not yet fully understood, and its potential as a therapeutic target warrants further investigation.
methodsBioinformatic analysis was performed using sequencing datas to evaluate clinical diagnostic and prognostic values of molecules. Biological functions were assessed using in vitro and in vivo experiments. Various techniques, including quantitative PCR, western blotting, immunohistochemistry, RNA immunoprecipitation, RNA pull-down, immunofluorescence, and luciferase reporter assays, were used to investigate the underlying molecular mechanisms.
resultsTAF9 was significantly overexpressed in HB tissues and correlated with poor prognosis. Both lncRNA938 and TAF9 promoted HB proliferation and metastasis. Mechanistically, lncRNA938 directly bound TAF9 and regulated its nuclear localization, while TAF9 activated TTK transcription via promoter binding. TTK inhibitors effectively reversed the epithelial-mesenchymal transition and malignant phenotypes induced by TAF9 overexpression.
conclusionThe lncRNA938-TAF9-TTK axis is a critical driver of HB progression. Targeting this axis, particularly through TTK inhibition, represents a novel therapeutic strategy against HB.
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