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

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

PROVIDER: PRJNA523175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10908033_1.fastq.gz	Fastqsanger.gz
	SRR10908033_2.fastq.gz	Fastqsanger.gz
	SRR10908034_1.fastq.gz	Fastqsanger.gz
	SRR10908034_2.fastq.gz	Fastqsanger.gz
	SRR10908035_1.fastq.gz	Fastqsanger.gz

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TRIB3 promotes MYC-associated lymphoma development through suppression of UBE3B-mediated MYC degradation.

Project description:The transcription factor MYC is deregulated in almost all human cancers, especially in aggressive lymphomas, through chromosomal translocation, amplification, and transcription hyperactivation. Here, we report that high expression of tribbles homologue 3 (TRIB3) positively correlates with elevated MYC expression in lymphoma specimens; TRIB3 deletion attenuates the initiation and progression of MYC-driven lymphoma by reducing MYC expression. Mechanistically, TRIB3 interacts with MYC to suppress E3 ubiquitin ligase UBE3B-mediated MYC ubiquitination and degradation, which enhances MYC transcriptional activity, causing high proliferation and self-renewal of lymphoma cells. Use of a peptide to disturb the TRIB3-MYC interaction together with doxorubicin reduces the tumor burden in MycEμ mice and patient-derived xenografts. The pathophysiological relevance of UBE3B, TRIB3 and MYC is further demonstrated in human lymphoma. Our study highlights a key mechanism for controlling MYC expression and a potential therapeutic option for treating lymphomas with high TRIB3-MYC expression.

| S-EPMC7725785 | biostudies-literature

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

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

2020-10-01 | GSE126258 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis

Project description:Pcgf6 suppresses Myc-induced lymphomagenesis

| PRJNA785557 | ENA

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

Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

Project description:Max is an obligate dimerization partner for the Myc transcription factors and for several repressors, such as Mnt, Mxd1-4 and Mga, collectively thought to antagonize Myc function in transcription and oncogenesis. Mga, in particular, is part of the variant Polycomb group repressive complex PRC1.6. Here, we show that ablation of the distinct PRC1.6 subunit Pcgf6 – but not Mga – accelerates Myc-induced lymphomagenesis in Eµ-myc transgenic mice. Unexpectedly, however, Pcgf6 loss shows no significant impact on transcriptional profiles, in neither pre-tumoral B-cells, nor lymphomas. Altogether, these data unravel an unforeseen, Mga- and PRC1.6-independent tumor suppressor activity of Pcgf6.

2021-12-05 | GSE189999 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

2021-12-05 | GSE189989 | GEO

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

Expression data from NB4 control shRNA cells and NB4 TRIB3 shRNA cells

Project description:To identify the top 20 up-regulated genes in NB4 TRIB3 shRNA cells in comparison with NB4 control shRNA cells, we examined the microarray gene expression profile of these groups above. Despite the fact that combined therapy of all-trans retinoic acid (ATRA) with arsenic trioxide (ATO) or chemotherapy dramatically improves the prognosis of patients with acute promyelocytic leukemia (APL), these regimens can cause systemic infections and secondary leukemias. Here we report that expression of the pseudokinase Tribble 3 (TRIB3) associates positively with APL progression and therapeutic resistance. The elevated TRIB3 expression promotes APL by interacting with PML-RARa and suppressing its sumoylation, ubiquitylation and degradation. This represses PML nuclear body assembly, p53-mediated senescence, cell differentiation, and supports cellular self-renewal. Genetically inhibiting Trib3 expression or disturbing the TRIB3/PML-RARa interaction produces potent therapeutic efficacy against APL and has synergic anti-APL effects when used in combination with ATRA or ATO by promoting PML-RARa degradation and PML expression. Our study provides new insight into APL pathogenesis and a new therapeutic option against APL.

2017-05-12 | GSE95637 | GEO

Regulation of the core pre-mRNA splicing machinery by MYC and PRMT5 is essential to sustain lymphomagenesis [B-cells]

Project description:Over-expressed MYC binds to virtually all active promoters within a cell, although with different binding affinities, and modulates gene expression, both positively and negatively. Here, we show that during lymphomagenesis in Eµ-myc transgenic mice, MYC directly up-regulates the transcription of the core snRNP assembly genes, including PRMT5, an arginine methyltransferase, that methylates Sm proteins as an early step in lymphomagenesis. This coordinated regulatory effect is direct and is critical for snRNP biogenesis, the maintenance of effective mRNA splicing and cellular viability in cycling cells, in either fibroblasts or B-cells. mRNA profiles of wild type and pre-tumoral eu-myc mice by deep sequencing, in triplicate, using Illumina NextSeq 500

2015-05-19 | E-GEOD-60188 | biostudies-arrayexpress

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