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KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma [RNA-Seq]

ABSTRACT: OCI_Ly1 cells treated with either DMSO or two different concentrations (150nM and 500nM) of the KDM4 inhibitor, JIB-04 were used for RNA-seq

ORGANISM(S): Homo sapiens

PROVIDER: GSE139183 | GEO | 2025/10/07

REPOSITORIES: GEO

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KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma [ChIP-Seq]

Project description:OCI_Ly1 cells treated with either DMSO or two different concentrations (150nM and 500nM) of the KDM4 inhibitor, JIB-04 were used for chip-seq

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Identification of genes modulated by JIB-04 in lung cancer cells

Project description:JIB-04 is an inhibitor of Jumonji histone demethylases identified through a cell based screen that measures the reactivation of an epigenetically silenced transgene. The active JIB-04 E-isomer shows selectivity for cancer vs. normal cells affecting both transcriptional patterns and cell viability in a cancer specific manner. H358 lung cancer cells or the patient matched HCC4017 (cancer) vs. HBEC30KT (immortalized normal) lung cell pair were treated with DMSO vehicle or 500nM E-isomer or 500 nM Z-isomer of JIB-04 for 4 h or 24 h and RNA extracted.

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KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma

Project description:This SuperSeries is composed of the SubSeries listed below.

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Histone Demethylases KDM4A and KDM4C Regulate Differentiation of Embryonic Stem Cells to Endothelial Cells.

Project description:Understanding epigenetic mechanisms regulating embryonic stem cell (ESC) differentiation to endothelial cells may lead to increased efficiency of generation of vessel wall endothelial cells needed for vascular engineering. Here we demonstrated that the histone demethylases KDM4A and KDM4C played an indispensable but independent role in mediating the expression of fetal liver kinase (Flk)1 and VE-cadherin, respectively, and thereby the transition of mouse ESCs (mESCs) to endothelial cells. KDM4A was shown to bind to histones associated with the Flk1 promoter and KDM4C to bind to histones associated with the VE-cadherin promoter. KDM4A and KDM4C were also both required for capillary tube formation and vasculogenesis in mice. We observed in zebrafish that KDM4A depletion induced more severe vasculogenesis defects than KDM4C depletion, reflecting the early involvement of KDM4A in specifying endothelial cell fate. These findings together demonstrate the essential role of KDM4A and KDM4C in orchestrating mESC differentiation to endothelial cells through the activation of Flk1 and VE-cadherin promoters, respectively.

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KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma

Project description:KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma

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Effect of conditional triple-knockout of Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c or overexpression of KDM4C/JMJD2C mutants with different phase separation ability on gene expression in mouse embryonic stem cells. [HiChIP]

Project description:To investigate the functions of JMJD2/KDM4 family in mouse embryonic stem cells (mESCs), we treat the the conditional triple-knockout mESCs of Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c with 4-hydroxytamoxifen (4-OHT) for 72h. Besides, to investigate whether JMJD2/KDM4 phase separation affects Enhancer-Promoter loops, we generated IDR-truncated JMJD2C/KDM4C (Mut) to disrupt its phase separation ability, and rescued it by by fusing two IDRs in other species (hIDR1 and hIDR2). Further, to investigate whether the functions of JMJD2/KDM4 are catalytic-dependent, we also generated catalytic mutants of JMJD2B and JMJD2C. We overexpressed those phase separation or catalytic mutants in the aboved mESCs separately and TKO endogenous Jmjd2 by adding 4-OHT 72h (for phase separation mutants) or 36h (for catalytic mutants).

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Project description:To investigate the functions of JMJD2/KDM4 family in mouse embryonic stem cells (mESCs), we treat the the conditional triple-knockout mESCs of Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c with 4-hydroxytamoxifen (4-OHT) for 72h. Further, to investigate whether JMJD2/KDM4 phase separation affects 2-Cell-like cells (2CLCs) induction, we generated IDR-truncated JMJD2C/KDM4C (Mut) to disrupt its phase separation ability, and rescued it by by fusing two IDRs in other species (hIDR1 and hIDR2). We overexpressed those phase separation mutants in the Zscan4-GFP::Mervl-tdTomoto mESCs separately.

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Project description:To investigate the functions of JMJD2/KDM4 family in mouse embryonic stem cells (mESCs), we treat the the conditional triple-knockout mESCs of Jmjd2a/Kdm4a, Jmjd2b/Kdm4b and Jmjd2c/Kdm4c with 4-hydroxytamoxifen (4-OHT) for 72h. Further, to investigate whether JMJD2/KDM4 phase separation affects chromatin binding of YY1, we generated IDR-truncated JMJD2C/KDM4C (Mut) to disrupt its phase separation ability, and rescued it by by fusing two IDRs in other species (hIDR1 and hIDR2). We overexpressed those phase separation mutants in the aboved mESCs separately and TKO endogenous Jmjd2 by adding 4-OHT 72h.

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KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma [ChIP-Seq]

Project description:KDM4A/KDM4C lysine demethylases sustain an oncogenic transcriptional program in diffuse large B-cell lymphoma [ChIP-Seq]

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