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Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation II

ABSTRACT: Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation II

PROVIDER: PRJNA1093417 | ENA |

REPOSITORIES: ENA

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Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation

Project description:Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation

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Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation III

Project description:Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation III

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Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation I

Project description:Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation I

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Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation III

Project description:MYC acts as a rheostat during plasma cell (PC) differentiation, linking B-cell activation to cell growth and division. Tight control over MYC is an essential feature of the network controlling differentiation. Deregulation of MYC is common in aggressive B-cell neoplasms, driving cellular transformation, and is often accompanied by apoptotic protection conferred by BCL2. Here we assess how acutely enforced MYC and BCL2 deregulation impacts on the ability of human B-cells to complete PC differentiation. In the context of a permissive state for PC differentiation such acute deregulation does not suffice to transform human B-cells. Instead MYC drives a sequence of metabolic and growth-related expression programs while suppressing the transition to immunoglobulin secretion and thus establishes an aberrant differentiation state. The ability of MYC to establish this aberrant state depends on MB0 and MBII of its transactivation domain. Dependence on MBII is profound and can be resolved to conserved residue W135.

2025-07-22 | GSE262807 | GEO

Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation II

2025-07-22 | GSE262805 | GEO

Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation I

2025-07-22 | GSE262804 | GEO

Hyperfunctioning MYC selectively redirects expression programs during human plasma cell differentiation

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

2025-07-22 | GSE262809 | GEO

MYC enhancer invasion promotes prognostic cancer type-specific gene programs through an epigenetic switch

Project description:The transcription factor MYC is overexpressed in most cancers, where it drives multiple hallmarks of cancer progression. MYC is known to promote oncogenic transcription by binding to active promoters. In addition, MYC has also been shown to invade distal enhancers when expressed at oncogenic levels, but this enhancer binding has been proposed to have low gene-regulatory potential. Here, we demonstrate that MYC enhancer binding directly promotes cancer type-specific gene programs predictive of poor patient prognosis. MYC induces transcription of enhancer RNA through recruitment of RNAPII, rather than regulating RNAPII pause-release as is the case at promoters. This is mediated by MYC-induced H3K9 demethylation by KDM3A and acetylation by GCN5, leading to enhancer-specific BRD4 recruitment through its bromodomains, which facilitates RNAPII recruitment. Thus, we propose that MYC drives prognostic cancer type-specific gene programs by promoting RNAPII recruitment to enhancers through induction of an epigenetic switch.

2023-11-30 | PXD039586 | Pride

Gene Amplification of Mediator Subunit 30 Redirects the MYC Transcriptional Program and Oncogenesis [Cut&Tag]

Project description:Understanding the molecular mechanisms underlying tumorigenesis is crucial for developing effective cancer therapies. Here, we investigate the common co-amplification of MED30 and MYC across diverse cancer types and its impact on oncogenic transcriptional programs. Transcriptional profiling of MYC and MED30 single or both overexpression/amplification revealed the over amount of MED30 lead MYC to a new transcriptional program that associate with poor prognosis. Mechanistically, MED30 overexpression/amplification recruits other Mediator components and binding of MYC to a small subset of novel genomic regulatory sites, changing the epigenetic marks and inducing the formation of new enhancers, which drive the expression of target genes crucial for cancer progression. In vivo studies in pancreatic ductal adenocarcinoma (PDAC) further validate the oncogenic potential of MED30, as its overexpression promotes tumor growth and can be attenuated by knockdown of MYC. Using another cancer type, MED30 knockdown reduces tumor growth particularly in MYC high-expressed glioblastoma (GBM) cell lines. Overall, our study elucidates the critical role of MED30 overexprssion in orchestrating oncogenic transcriptional programs and highlights its potential as a therapeutic target for MYC-amplified cancer.

2024-05-30 | GSE264275 | GEO