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Non-oncogene addiction to SIRT3 plays a critical role in lymphomagenesis

ABSTRACT: Non-oncogene addiction to SIRT3 plays a critical role in lymphomagenesis

PROVIDER: PRJNA541280 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9017340_1.fastq.gz	Fastqsanger.gz
	SRR9017340_2.fastq.gz	Fastqsanger.gz
	SRR9017350_1.fastq.gz	Fastqsanger.gz
	SRR9017350_2.fastq.gz	Fastqsanger.gz
	SRR9017360_1.fastq.gz	Fastqsanger.gz

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Non-oncogene addiction to SIRT3 plays a critical role in lymphomagenesis

Project description:Diffuse large B-cell lymphomas (DLBCLs) are genetically heterogeneous and highly proliferative neoplasms derived from germinal center (GC) B-cells. Herein, we show that DLBCLs are dependent on mitochondrial lysine deacetylase SIRT3 for proliferation, survival, self-renewal, and tumor growth in vivo regardless of disease subtype and genetics. SIRT3 knockout attenuated B-cell lymphomagenesis in VavP-Bcl2 mice without affecting normal GC formation. Mechanistically, SIRT3 depletion impaired glutamine flux to the TCA cycle via glutamate dehydrogenase and reduction in acetyl-CoA pools, which in turn induce autophagy and cell death. We developed a mitochondrial-targeted Class I sirtuin inhibitor, YC8-02, that phenocopied the effects of SIRT3 depletion and killed DLBCL cells. SIRT3 is thus a metabolic non-oncogene addiction and therapeutic target for DLBCLs.

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Non-oncogene Addiction to SIRT3 Plays a Critical Role in Lymphomagenesis.

Project description:Diffuse large B cell lymphomas (DLBCLs) are genetically heterogeneous and highly proliferative neoplasms derived from germinal center (GC) B cells. Here, we show that DLBCLs are dependent on mitochondrial lysine deacetylase SIRT3 for proliferation, survival, self-renewal, and tumor growth in vivo regardless of disease subtype and genetics. SIRT3 knockout attenuated B cell lymphomagenesis in VavP-Bcl2 mice without affecting normal GC formation. Mechanistically, SIRT3 depletion impaired glutamine flux to the TCA cycle via glutamate dehydrogenase and reduction in acetyl-CoA pools, which in turn induce autophagy and cell death. We developed a mitochondrial-targeted class I sirtuin inhibitor, YC8-02, which phenocopied the effects of SIRT3 depletion and killed DLBCL cells. SIRT3 is thus a metabolic non-oncogene addiction and therapeutic target for DLBCLs.

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