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KDM6A Regulates Immunogenicity of Multiple Myeloma (ChIP-seq)

ABSTRACT: We created isogenic mutiple myeloma and mouse embryonic fibroblast cell lines disrupted for KDM6A using CRISPR editing and Cre-mediated deletion. To detect KDM6A we inserted a dual HA tag sequence into the C-terminal of KDM6A by CRISPR-mediated editing. We also created one isogenic cell line harboring a jmjD-dead KDM6A where 2 amino acids essential for KDM6A enzymatic activity, H1146 and E1148 , were replaced with alanine residues

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE244510 | GEO | 2024/10/01

REPOSITORIES: GEO

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KDM6A Regulates Immunogenicity of Multiple Myeloma (ATAC-seq)

Project description:We created isogenic mutiple myeloma cell lines disrupted for KDM6A using CRISPR-mediated editing.

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KDM6A Regulates Immunogenicity of Multiple Myeloma (RNA-seq)

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Project description:Using a CRISPR-based autochthonous SCLC GEMM to study the consequences of KDM6A/UTX inactivation, we found that KDM6A inactivation induced plasticity from ASCL1 to NEUROD1 resulting in SCLC tumors with open chromatin at the NEUROD1 promoter that express both ASCL1 and NEUROD1. Mechanistically, KDM6A binds and maintains ASCL1 target genes in an active chromatin state with its loss decreasing H3K4me1 and increasing H3K27me3 at enhancers of neuroendocrine genes leading to a cell state that is primed for ASCL1 to NEUROD1 subtype switching. This work identifies KDM6A as an epigenetic regulator that controls ASCL1 to NEUROD1 subtype plasticity and provides a novel autochthonous SCLC GEMM to model ASCL1 and NEUROD1 subtype heterogeneity and plasticity, which is found in 35-40% of human SCLCs.

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