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Gcn5 transcriptional activation of Myc-induced genes promotes B-cell lymphomagenesis

ABSTRACT: Gcn5 transcriptional activation of Myc-induced genes promotes B-cell lymphomagenesis

PROVIDER: PRJNA645138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12185474_1.fastq.gz	Fastqsanger.gz
	SRR12185474_2.fastq.gz	Fastqsanger.gz
	SRR12185475_1.fastq.gz	Fastqsanger.gz
	SRR12185475_2.fastq.gz	Fastqsanger.gz
	SRR12185476_1.fastq.gz	Fastqsanger.gz

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Gcn5 transcriptional activation of Myc-induced genes promotes B-cell lymphomagenesis

Project description:Purpose: In this study we sought to elucidate whether Gcn5 cooperates with Myc to induce the formation of lymphoma using an in vivo model, the Eµ-Myc mouse. In order to define the molecular mechanisms for how Gcn5 contributes to lymphoma development upon overexpression of Myc, we performed RNA-seq analyses on total RNA isolated from CD19+ B cells sorted from spleens of 5-6-week-old wild-type, Eµ-Myc, and Eµ-Myc; Gcn5Fx/Fx mice. Conclusions: Loss of Gcn5 not only ameliorates dysregulation of the cell cycle caused by Myc overexpression, but also affects Myc-induced pathways related to cancer cell growth.

2020-12-29 | GSE154108 | GEO

Transcriptional Activation of MYC-Induced Genes by GCN5 Promotes B-cell Lymphomagenesis.

Project description:Overexpression of the MYC oncoprotein is an initiating step in the formation of several cancers. MYC frequently recruits chromatin-modifying complexes to DNA to amplify the expression of cancer-promoting genes, including those regulating cell cycle, proliferation, and metabolism, yet the roles of specific modifiers in different cancer types are not well defined. Here, we show that GCN5 is an essential coactivator of cell-cycle gene expression driven by MYC overexpression and that deletion of Gcn5 delays or abrogates tumorigenesis in the Eμ-Myc mouse model of B-cell lymphoma. Our results demonstrate that Gcn5 loss impacts both expression and downstream functions of Myc. SIGNIFICANCE: Our results provide important proof of principle for Gcn5 functions in formation and progression of Myc-driven cancers, suggesting that GCN5 may be a viable target for development of new cancer therapies.

| S-EPMC7744430 | biostudies-literature

Pcgf6 suppresses Myc-induced lymphomagenesis

Project description:Pcgf6 suppresses Myc-induced lymphomagenesis

| PRJNA785557 | ENA

TRIB3 Promotes C-Myc-Associated Lymphomagenesis through Inhibition of UBE3B-Mediated c-Myc Degradation

Project description:TRIB3 Promotes C-Myc-Associated Lymphomagenesis through Inhibition of UBE3B-Mediated c-Myc Degradation

| PRJNA523175 | ENA

IL-6 promotes MYC-induced B cell lymphomagenesis independent of STAT3

Project description:IL-6 promotes MYC-induced B cell lymphomagenesis independent of STAT3

| PRJNA693547 | ENA

Pin1 is required for sustained B cell proliferation upon oncogenic activation of Myc

Project description:The c-myc proto-oncogene is activated by translocation in Burkitt's lymphoma and substitutions in codon 58 stabilize the Myc protein or augment its oncogenic potential. In wild-type Myc, phosphorylation of Ser 62 and Thr 58 provide a landing pad for the peptidyl prolyl-isomerase Pin1, which in turn promotes Ser 62 dephosphorylation and Myc degradation. However, the role of Pin1 in Myc-induced lymphomagenesis remains unknown. We show here that genetic ablation of Pin1 reduces lymphomagenesis in EÂµ-myc transgenic mice. In both Pin1-deficient B-cells and MEFs, the proliferative response to Myc was selectively impaired, with no alterations in Myc-induced apoptosis or mitogen-induced cell cycle entry. This proliferative defect wasn't attributable to alterations in either Ser 62 phosphorylation or Myc-regulated transcription, but to the indirect activation of an Arf-p53 dependent cytostatic response. Pin1 silencing in lymphomas retarded disease progression in mice, making Pin1 an attractive therapeutic target in Myc-driven tumors. RNAseq samples of Pin1+/+ control (n=4), Pin1 -/- control (n=2), Pin1+/+ EÂµ-myc pre-tumoral (n=3), and Pin1-/- EÂµ-myc pre-tumoral (n=4) B cells.

2016-06-14 | E-GEOD-77482 | biostudies-arrayexpress

IL-6 promotes MYC-induced B cell lymphomagenesis independent of STAT3

Project description:The inflammatory cytokine IL-6 is known to play a causal role in the promotion of cancer, although the underlying mechanisms remain to be completely understood. Interplay between endogenous and environmental cues determines the fate of cancer development. The Eμ-myc transgenic mouse expresses elevated levels of c-Myc in the B cell lineage and develops B cell lymphomas with associated mutations in p53 or other genes linked to apoptosis. We generated Eμ-myc mice that either lacked the IL-6 gene, or lacked the STAT3 gene specifically in B cells to determine the role of the IL-6/JAK/STAT3 pathway in tumor development. Using the Eμ-myc lymphoma mouse model, we demonstrate that IL-6 is a critical tumor promoter during early stages of B cell lymphomagenesis. IL-6 is shown to inhibit the expression of tumor suppressors, notably BIM and PTEN, thereby advancing MYC-driven B cell tumorigenesis. Several miRNAs known to target BIM and PTEN are upregulated by IL-6 and likely lead to the stable suppression of pro-apoptotic pathways early during the tumorigenic process. STAT3, a classical downstream effector of IL-6, appears dispensable for Eμ-myc driven lymphomagenesis. We conclude that the growth-promoting and anti-apoptotic mechanisms activated by IL-6 are critically involved in Eμ-myc driven tumor initiation and progression, but the B cell intrinsic expression of STAT3 is not required.

2021-02-02 | GSE165205 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

Project description:Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

| PRJNA785559 | ENA

Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

Project description:Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

| PRJNA785540 | ENA

Pin1 is required for sustained B cell proliferation upon oncogenic activation of Myc

Project description:The c-myc proto-oncogene is activated by translocation in Burkitt's lymphoma and substitutions in codon 58 stabilize the Myc protein or augment its oncogenic potential. In wild-type Myc, phosphorylation of Ser 62 and Thr 58 provide a landing pad for the peptidyl prolyl-isomerase Pin1, which in turn promotes Ser 62 dephosphorylation and Myc degradation. However, the role of Pin1 in Myc-induced lymphomagenesis remains unknown. We show here that genetic ablation of Pin1 reduces lymphomagenesis in Eµ-myc transgenic mice. In both Pin1-deficient B-cells and MEFs, the proliferative response to Myc was selectively impaired, with no alterations in Myc-induced apoptosis or mitogen-induced cell cycle entry. This proliferative defect wasn't attributable to alterations in either Ser 62 phosphorylation or Myc-regulated transcription, but to the indirect activation of an Arf-p53 dependent cytostatic response. Pin1 silencing in lymphomas retarded disease progression in mice, making Pin1 an attractive therapeutic target in Myc-driven tumors.

2016-06-14 | GSE77482 | GEO

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