ArticleNature communications2024
Transposable elements-mediated recruitment of KDM1A epigenetically silences HNF4A expression to promote hepatocellular carcinoma.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Ligand-dependent reprogramming of HNF4A expression and function suppresses multistep hepatocarcinogenesis.Molecular therapy. Oncology · 2026Article
- Exploring and experimental validation of SLC7A11 and ferroptosis related prognostic genes in non-small cell lung cancer using bulk RNA sequencing and single-cell RNA sequencing.Biology direct · 2026Article
- Crosstalk BetweenCancers · 2026Review
- Epigenetic and post-translational regulatory networks of ferroptosis in the tumor immune microenvironment.Experimental hematology & oncology · 2026Review
- Transposable Element Dysregulation in Hepatocellular Carcinoma: Epigenetic Mechanisms, Immune Remodeling, and Translational Opportunities.Journal of hepatocellular carcinoma · 2026Review
- HERVH-derived eRNA activates a super-enhancer-driven ALDH1A3/SAT1 axis to promote ferroptosis escape and pancreatic cancer development.Science advances · 2025Article
- HSPB1/KDM1 A facilitates ANXA2 expression via hypomethylated DNA promoter to inhibit ferroptosis and enhance gemcitabine resistance in pancreatic cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Identification of immunosuppressive CD4Discover oncology · 2025Article
- Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025Review
- Shedding light on DNA methylation and its clinical implications: the impact of long-read-based nanopore technology.Epigenetics & chromatin · 2024Review
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Authors and funding
9 authors.
Funding
Abstract
Transposable elements (TEs) contribute to gene expression regulation by acting as cis-regulatory elements that attract transcription factors and epigenetic regulators. This research aims to explore the functional and clinical implications of transposable element-related molecular events in hepatocellular carcinoma, focusing on the mechanism through which liver-specific accessible TEs (liver-TEs) regulate adjacent gene expression. Our findings reveal that the expression of HNF4A is inversely regulated by proximate liver-TEs, which facilitates liver cancer cell proliferation. Mechanistically, liver-TEs are predominantly occupied by the histone demethylase, KDM1A. KDM1A negatively influences the methylation of histone H3 Lys4 (H3K4) of liver-TEs, resulting in the epigenetic silencing of HNF4A expression. The suppression of HNF4A mediated by KDM1A promotes liver cancer cell proliferation. In conclusion, this study uncovers a liver-TE/KDM1A/HNF4A regulatory axis that promotes liver cancer growth and highlights KDM1A as a promising therapeutic target. Our findings provide insight into the transposable element-related molecular mechanisms underlying liver cancer progression.
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