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Polycomb group ring finger protein 6 suppresses Myc-induced lymphomagenesis.

ABSTRACT: 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.

SUBMITTER: Tanaskovic N

PROVIDER: S-EPMC9012912 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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Polycomb group ring finger protein 6 suppresses Myc-induced lymphomagenesis.

Tanaskovic Nina N Dalsass Mattia M Filipuzzi Marco M Ceccotti Giorgia G Verrecchia Alessandro A Nicoli Paola P Doni Mirko M Olivero Daniela D Pasini Diego D Koseki Haruhiko H Sabò Arianna A Bisso Andrea A Amati Bruno B

Life science alliance 20220414 8

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-<i>myc</i> transgenic mice. Unexpectedly, however, Pcgf6 loss shows no signifi ...[more]

PMID: 35422437

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FoxO3 suppresses Myc-driven lymphomagenesis.

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Pcgf6 suppresses Myc-induced lymphomagenesis

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

2021-12-05 | GSE190000 | GEO

Pcgf6 suppresses Myc-induced lymphomagenesis

Project description:Pcgf6 suppresses Myc-induced lymphomagenesis

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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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Ring finger protein 126 (RNF126) suppresses ionizing radiation-induced p53-binding protein 1 (53BP1) focus formation.

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Pcgf6 suppresses Myc-induced lymphomagenesis [RNA-seq]

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

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Pcgf6 suppresses Myc-induced lymphomagenesis [ChIP-seq]

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

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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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