ArticleCellular oncology (Dordrecht, Netherlands)2026
Super-enhancer-associated lncRNA HDAC11-AS1 aggravates hepatocellular carcinoma progression by modulating HDAC11 and NUP210 expression via promoting super-enhancer activity.
Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeHepatocellular carcinoma (HCC), a malignancy driven by multifaceted genetic and epigenetic mechanisms, is the leading cause of cancer deaths worldwide. Long non-coding RNAs (lncRNAs), particularly super-enhancer-associated lncRNAs (SE-lncRNAs), have emerged as critical regulators of tumorigenesis.
methodsIn our study, we explored the expression of super-enhancer (SE)-associated lncRNA (seRNA) in HCC and investigated the role of a SE-lncRNA, HDAC11-AS1, in the progression of HCC. HCC-specific SE-lncRNAs were identified by H3K27ac ChIP-seq data (from ENCODE database) of Huh7, HepG2, and normal liver tissues using the ROSE algorithm. HDAC11-AS1 overexpression was validated in 36 pairs of HCC patient samples and adjacent tissues. The effects of HDAC11-AS1 on HCC proliferation and migration was analyzed in vitro and in vivo by overexpression or knockdown of HDAC11-AS1. Co-expression genes analysis of HDAC11-AS1, qPCR, western blot analysis and immunohistochemistry (IHC) were used to detect the regulation of Histone Deacetylase 11(HDAC11) and Nucleoporin 210 (NUP210).ChIA-PET data analysis, RNA pulldown and RNA immunoprecipitation (RIP) were used to explore the interaction between HDAC11-AS1 and tanscription factor (YY1)/cofactors (EP300 and SMC3).
resultsIn this study, we identified HDAC11-AS1, a SE-lncRNA significantly overexpressed in HCC tissues and associated with poor prognosis. Downregulation of HDAC1-AS1 suppressed proliferation and migration of HCC in vitro and in vivo. Mechanistically, HDAC11-AS1 as a pivotal SE-lncRNA driving HCC progression through transcriptional regulation of HDAC11 and NUP210 by interacting with transcription factor YY1 and cofactor (EP300 and SMC3) in stabilizing enhancer-promoter looping.
conclusionsOur findings reveal that HDAC11-AS1 functions as a molecular scaffold that stabilizes enhancer-promoter (E-P) looping, thereby promoting super-enhancer activity and the subsequent transcription of oncogenic drivers.
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