ArticleThe Journal of biological chemistry2026
Dysregulated HELLS expression alters cellular processes and serves as a potential prognostic marker in acute myeloid leukemia.
Article in The Journal of biological chemistry, 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
Spatiotemporal gene expression is regulated by the SNF2 family of ATPases that remodel chromatin, among which helicase lymphoid-specific (HELLS) play an essential role in DNA-templated processes. Analysis from cancer databases revealed HELLS upregulation in several cancers, including acute myeloid leukemia (AML). Using an in vitro myeloid differentiation model, we found that HELLS deficiency promotes myeloid differentiation, apoptosis, cell-cycle arrest, and chromatin instability. Furthermore, HELLS deficiency enhanced myeloid differentiation and apoptosis in HL-60 cells when treated with chemotherapy drugs, including 5-azacytidine, cytarabine, and doxorubicin. Epigenetically, loss of HELLS reduced active histone mark (H3K4me3) and enhanced repressive promoter (H3K27me3), active enhancer (H3K27ac) marks, and chromatin accessibility. Transcriptomic analysis of BeatAML data and bioinformatics analysis revealed that HELLS upregulation is associated with adverse prognosis, as defined by the ELN-2017 classification, and significantly poorer survival. Classification of AML patients into HELLS
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