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NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2.

ABSTRACT: NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2.

PROVIDER: PRJNA1027238 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26363252_1.fastq.gz	Fastqsanger.gz
	SRR26363252_2.fastq.gz	Fastqsanger.gz
	SRR26373152_1.fastq.gz	Fastqsanger.gz
	SRR26373152_2.fastq.gz	Fastqsanger.gz
	SRR26363253_1.fastq.gz	Fastqsanger.gz

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NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2 [AS_CR]

Project description:Chromosomal translocation t(4;14), a driver of NSD2 overexpression, remains a negative prognostic factor in multiple myeloma (MM). A genome-wide CRISPR screen in MM cells identified adenylate kinase 2 (AK2) as an NSD2-driven vulnerability. AK2 depletion in t(4;14) MM cells inhibited cell growth in vitro and in vivo, impaired protein folding in the ER and increased sensitivity to proteasome inhibition, consistent with a defect in shuttling ATP from the mitochondria. Moreover, AK2 suppression decreased intracellular NADP(H) critical for thioredoxin reduction, which is key for deoxyribonucleotides (dNTP) synthesis, leading to DNA replication stress and apoptosis. The increased dependence on AK2 was attributed to insufficient creatine production due to NSD2-mediated diversion of one-carbon metabolism to the epigenome and away from S-adenosylmethionine dependent creatine synthesis. Correspondingly, supplementation with creatine restored NADP(H) levels and rescued AK2-deficient cells from apoptosis. These findings revealed a novel metabolic susceptibility and promising therapeutic strategy for targeting t(4;14) MM.

2024-10-07 | GSE245148 | GEO

NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2 [AS_RS]

2024-10-07 | GSE245149 | GEO

NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2 [AS_RS]

Project description:NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2 [AS_RS]

| PRJNA1027251 | ENA

NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2 [AS_CR]

Project description:NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2 [AS_CR]

| PRJNA1027240 | ENA

NSD2 Overexpression in Myeloma Enhances Dependency on Mitochondrial High Energy Phosphate Transport Facilitated by Adenylate Kinase 2.

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

2024-10-07 | GSE245150 | GEO

Defining the NSD2 interactome: PARP1 PARylation reduces NSD2 histone methyltransferase activity and impedes chromatin binding

Project description:NSD2 is a histone methyltransferase that specifically dimethylates histone H3 lysine 36 (H3K36me2), a modification associated with gene activation. Dramatic overexpression of NSD2 in t(4;14) multiple myeloma (MM) and an activating mutation of NSD2 discovered in acute lymphoblastic leukemia (ALL) are significantly associated with altered gene activation, transcription and DNA damage repair. The partner proteins through which NSD2 may influence critical cellular processes remain poorly defined. In this study, we utilized proximity-based labelling (BioID) combined with label-free quantitative mass spectrometry to identify high confidence NSD2 interacting partners in MM cells.

2019-06-27 | PXD013759 | Pride

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming

Project description:This SuperSeries is composed of the following subset Series: GSE29146: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP] GSE29147: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi] GSE29148: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO] GSE29150: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction] Refer to individual Series

2011-11-29 | E-GEOD-29305 | biostudies-arrayexpress

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi]

Project description:NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming. Genome-wide expression profiling of KMS11 cells stably transduced with control vector in comparison to two independent shRNAs against NSD2. Each cell line is tested in duplicate.

2011-11-29 | E-GEOD-29147 | biostudies-arrayexpress

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction]

Project description:NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming. Genome-wide expression profiling of p19ARF-/- mouse embryonic fibroblasts stably transduced with control vector or wild-type NSD2. Each cell line is tested in triplicate.

2011-11-29 | E-GEOD-29150 | biostudies-arrayexpress

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO]

Project description:NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming. Genome-wide expression profiling of KMS11 and t(4;14) translocation knockout (TKO) cells. Each cell line is tested in triplicate.

2011-11-29 | E-GEOD-29148 | biostudies-arrayexpress

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