ArticleCell death & disease2025
ACTL6A depletion induces KLF4-mediated anti-tumorigenic effects in colorectal cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Overexpression of ACTL6A is associated with poor prognosis in gastric cancer, and nuclear level is an independent predictor.Translational cancer research · 2026Article
- Mechanoepigenetic Targeting of Histone Methyltransferase EZH2 Increases Potential of Scalable Manufacturing in Human Derived Primary Mesenchymal Stromal Cells.bioRxiv : the preprint server for biology · 2025Article
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7 authors.
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Abstract
ACTL6A, a subunit of the SWI/SNF and INO80 chromatin remodeling complexes, is frequently overexpressed in various cancers, and its depletion attenuates cell proliferation in colorectal cancer (CRC). However, the epigenetic mechanisms underlying ACTL6A function remain poorly understood. Here, we aimed to elucidate how ACTL6A regulates chromatin accessibility and gene expression in CRC. Integrated multi-omics analyses revealed that ACTL6A deficiency alters chromatin accessibility and upregulates P53 pathway-related genes, accompanied by the recruitment of SWI/SNF and INO80 complexes. Mechanistically, ACTL6A depletion enhances KLF4 binding at newly accessible regions, where it cooperates with these chromatin remodeling complexes to activate P53 pathway-related genes and induce apoptosis. ACTL6A contributes to CRC cell proliferation by inhibiting the KLF4-mediated transcriptional activation of tumor-suppressive genes. Thus, our findings highlight that targeting ACTL6A may serve as a promising therapeutic strategy in CRC.
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