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Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

ABSTRACT: Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

PROVIDER: PRJNA785559 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17096512_1.fastq.gz	Fastqsanger.gz
	SRR17096512_2.fastq.gz	Fastqsanger.gz
	SRR17096513_1.fastq.gz	Fastqsanger.gz
	SRR17096513_2.fastq.gz	Fastqsanger.gz
	SRR17096514_1.fastq.gz	Fastqsanger.gz

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Pcgf6 suppresses Myc-induced lymphomagenesis

Project description:Pcgf6 suppresses Myc-induced lymphomagenesis

| PRJNA785557 | ENA

Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

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

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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]

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Pcgf6 suppresses Myc-induced lymphomagenesis

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

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The IKK2/NF-kB-pathway suppresses MYC-induced lymphomagenesis

Project description:Abstract. Deregulated c-MYC is found in a variety of cancers where it promotes proliferation as well as apoptosis. In many hematological malignancies enhanced NF-kB exerts prosurvival functions. Here we investigated the role of NF-kB in mouse and human c-MYC-transformed lymphomas. The NF-kB-pathway is extinguished in murine lymphoma cells and extrinsic stimuli typically inducing NF-kB activity fail to activate this pathway. Genetic activation of the NF-kB pathway induces apoptosis in these cells, while inhibition of NF-kB by an IkBa superrepressor provides a selective advantage in vivo. Furthermore, in human Burkitt´s lymphoma cells we find that NF-kB activation induces apoptosis. NF-kB upregulates Fas and predisposes to Fas-induced cell death, which is caspase 8 mediated and can be prevented by CFLAR overexpression. We conclude that c-MYC overexpression sensitizes cells to NF-kB-induced apoptosis and persistent inacvtivity of NF-kB signaling is a prerequisite for MYC-mediated tumorigenesis. We could also show that low immunogenicity and Fas insensitivity of MYC driven lymphoma cells is reversed by activation of NF-kB. Our observations provide a molecular explanation for the described absence of the NF-kB signaling in Burkitt´s lymphoma and question the applicability of NF-kB inhibitors as candidates for treatment of this cancer.

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

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

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

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

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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.

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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

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