Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ACCESS DATA

Json Xml

Dataset's files

Source:

			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

Items per page:

1 - 5 of 127

Similar Datasets

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

| PRJNA302297 | ENA

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

Oncogene addiction to GNAS in GNASR201 mutant tumors

Project description:Oncogene addiction to GNAS in GNASR201 mutant tumors

| PRJNA859019 | ENA

Oncogene-like addiction to aneuploidy in human cancers

Project description:Oncogene-like addiction to aneuploidy in human cancers

| PRJNA921841 | ENA

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

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

2014-05-29 | GSE57507 | GEO

Transcriptional Targeting Of Oncogene Addiction In Medullary Thyroid Cancer

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

| PRJNA464052 | ENA

A transcription factor addiction imposed by an oncogene promoter sequence

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

| PRJNA474222 | ENA