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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.

2019-10-08 | GSE130751 | GEO

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.

| S-EPMC7534582 | biostudies-literature

Mechanism of Oncogene Addiction

Project description:Mechanism of Oncogene Addiction

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An oncogene addiction phosphorylation signature and its derived scores inform tumor responsiveness to targeted therapies

Project description:Oncogene addiction provides important therapeutic opportunities for precision oncology treatment strategies. To date the cellular circuitries associated with driving oncoproteins, which eventually establish the phenotypic manifestation of oncogene addiction remain largely unexplored. We employed a targeted mass spectrometry approach to systematically explore alterations in 116 phosphosites related to oncogene signaling and its intersection with the DDR following inhibition of the addicting oncogene alone or in combination with irradiation in MET-, EGFR-, ALK- or BRAF (V600)-positive cancer models and ex vivo non-small cell lung cancer patient organotypic cultures. We identified an ‘oncogene addiction phosphorylation signature’ (OAPS) consisting of 8 protein phosphorylations (ACLY S455, IF4B S422, IF4G1 S1231, LIMA1 S490, MYCN S62, NCBP1 S22, P3C2A S259 and TERF2 S365) that are significantly suppressed upon targeted oncogene inhibition solely in addicted cell line models and patient tissues. We show that the OAPS is present in patient tissues and the OAPS-derived score strongly correlates with the ex vivo responses to targeted treatments.

2023-03-11 | PXD037406 | Pride

The role of microRNA miR-17-92 in MYC oncogene addiction

Project description:miR-17-92 mediates the MYC oncogene addiction in a conditional mouse lymphoma model. To identify targets of miR-17-92 in this model, miR-17-92 was expressed in the conditional lymphoma cell lines using MSCV-puro. Both control and miR-17-92-expressing conditional lymphoma cell lines were treated with doxycycline (DOX) (20ng/ml) for 48 hours to shut off MYC expression.

2014-05-29 | E-GEOD-57507 | biostudies-arrayexpress

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Project description:Transcriptional Targeting Of Oncogene Addiction In Medullary Thyroid Cancer

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Lymphomas that recur after MYC suppression continue to exhibit oncogene addiction

Project description:The suppression of oncogenic levels of MYC is sufficient to induce sustained tumor regression associated with proliferative arrest, differentiation, cellular senescence and/or apoptosis, a phenomenon known as oncogene addiction. However, after prolonged inactivation of MYC in a conditional transgenic mouse model of Em-tTA/tetO-MYC T-acute lymphomablastic lymphoma (T-ALL), some of the tumors recur, recapitulating what is frequently observed in human tumors in response to targeted therapies. Here we report that these recurring lymphomas express high levels of either transgenic or endogenous Myc suggesting that tumors continue to be addicted to oncogenic levels of MYC. Many of the recurring lymphomas (76%) harbored mutations in the tetracycline transactivator (tTA) resulting in expression of the MYC transgene even in the presence of doxycycline. Many of the remaining recurring tumors expressed high levels of endogenous Myc which was in some cases associated with a genomic rearrangement of the endogenous Myc locus or overexpression of Notch1. Gene expression profiling confirmed that the primary and recurring tumors have highly similar transcriptomes. Importantly, shRNA-mediated suppression of the high levels of MYC in recurring tumors elicited both suppression of proliferation and increased apoptosis confirming that these tumors remain oncogene addicted. These results suggest that tumors caused by MYC overexpression remain addicted to high levels of expression of this oncogene. 13 samples, no replicates included

2011-09-23 | E-GEOD-32341 | biostudies-arrayexpress

A transcription factor addiction imposed by an oncogene promoter sequence

Project description:A transcription factor addiction imposed by an oncogene promoter sequence

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Transcription profiling of mouse lymphomagenesis induced by conditional expression of transgenic c-Myc oncogene in six different tumor cell lines

Project description:Lymphomagenesis was induced by conditional expression of transgenic c-Myc oncogene. Profile of genes expressed in tumor cells was compared with profile of genes in the same cell line treated for 12 hours with doxycycline to abrogate expression of transgenic c-Myc. Six different tumor cell lines were tested.

2004-09-17 | E-MEXP-169 | biostudies-arrayexpress

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