ArticleCell reports2025
Menin-MLL1 complex cooperates with NF-Y to promote hepatocellular carcinoma survival.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MEN1/menin deficiency suppresses hepatocellular carcinogenesis via disrupting mitophagy-mediated mitochondrial homeostasis.Autophagy · 2026Article
- Massively parallel assessment of gene regulatory activity at human cortical-structure-associated variants.Nature neuroscience · 2026Article
- Chromatin State Distinguishes Injury-Responsive from State-Stabilizing Transcriptional Programs in Hybrid Hepatocytes.bioRxiv : the preprint server for biology · 2026Article
- CRISPR Screening in Hepatocellular Carcinoma: From Tumor Progression to Immune Evasion and Therapeutic Resistance.International journal of molecular sciences · 2026Review
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6 authors.
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Abstract
Chromatin regulators are frequently mutated or aberrantly expressed in hepatocellular carcinoma (HCC), suggesting that the dysregulation of chromatin is a key feature driving liver cancer. In this study, using an epigenome-focused CRISPR screen in two-dimensional (2D) and three-dimensional (3D) conditions, we find the subunits of the menin-MLL1 complex to be among the strongest candidates for HCC survival. Inhibition of the menin-MLL1 interaction leads to global changes in occupancy of the complex with concomitant decreases in H3 lysine 4 trimethylation (H3K4me3), accessibility, and gene expression. Newly opened chromatin sites not bound by menin-MLL1 are associated with the recruitment of the pioneer transcription factor complex NF-Y yet remain embedded in silent chromatin domains, suggesting that they are primed for expression. A CRISPR-Cas9 screen of chromatin regulators in the presence of menin inhibitor SNDX-5613 reveals a significantly increased cell death when combined with NFYB knockout. Together, these data show that menin-MLL1 is necessary for HCC cell survival and cooperates with NF-Y to regulate oncogenic gene transcription.
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