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Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [Hi-C]

ABSTRACT: Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [Hi-C]

PROVIDER: PRJNA1111556 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29025667_1.fastq.gz	Fastqsanger.gz
	SRR29025667_2.fastq.gz	Fastqsanger.gz
	SRR29025668_1.fastq.gz	Fastqsanger.gz
	SRR29025668_2.fastq.gz	Fastqsanger.gz
	SRR29025669_1.fastq.gz	Fastqsanger.gz

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Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma

Project description:Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma

| PRJNA1111545 | ENA

Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [Hi-C]

Project description:Medulloblastoma is the most common malignant brain tumor of childhood. The highest-risk tumors are driven by recurrent Myc amplifications (Myc-MB) and experience poorer outcomes despite intensive multimodal therapy. The Myc transcription factor defines core regulatory circuitry for these tumors and acts to broadly amplify downstream pro-survival transcriptional programs. Therapeutic targeting of Myc directly has proven elusive, but inhibiting transcriptional cofactors may present an indirect means of drugging the oncogenic transcriptional circuitry sustaining Myc-MB. Independent CRISPR-Cas9 screens were pooled to identify conserved dependencies in Myc-MB. We performed chromatin conformation capture (Hi-C) from primary patient Myc-MB samples to map enhancer-promoter interactions. We then treated in vitro and xenograft models with the dual CDK9/7 inhibitor zotiraciclib to evaluate effect on Myc-driven programs and tumor growth. Eight CRISPR-Cas9 screens performed across three independent labs identify CDK9 as a conserved dependency in Myc-MB. Myc-MB cells are susceptible to CDK9 inhibition, which is synergistic with concurrent inhibition of CDK7. The dual CDK9/7 inhibitor zotiraciclib disrupts enhancer-promoter activity in Myc-MB and downregulates Myc-driven transcriptional programs, exerting potent anti-tumor effect.

2024-11-14 | GSE267471 | GEO

Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [RNA-seq]

Project description:Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [RNA-seq]

| PRJNA1111558 | ENA

Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [CUT&RUN]

Project description:Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [CUT&RUN]

| PRJNA1111557 | ENA

Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [CUT&RUN]

2024-11-14 | GSE267470 | GEO

Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma [RNA-seq]

2024-11-14 | GSE267469 | GEO

Dual targeting of processive transcription for Myc-driven circuitry in medulloblastoma

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

2024-11-14 | GSE267473 | GEO

O-GlcNAcylation Promotes Cerebellum Development and Medulloblastoma Oncogenesis via SHH Signaling

Project description:Sonic hedgehog (Shh) signaling plays a critical role in regulating cerebellum development by maintaining the physiological proliferation of granule neuron precursors (GNPs), and its dysregulation leads to the oncogenesis of medulloblastoma. O-GlcNAcylation (O-GlcNAc) of proteins is an emerging regulator of brain function that maintains normal development and neuronal circuitry. Here, we demonstrate that O-GlcNAc transferase (OGT) in GNPs mediate the cerebellum development, and the progression of the Shh-subgroup of medulloblastoma. Specifically, OGT regulates the proliferation of GNPs by activating the Shh signaling pathway via O-GlcNAcylation at S355 of GLI family zinc finger 2 (Gli2), which in turn promotes its deacetylation and transcriptional activity via dissociation from p300, a histone acetyltransferases (HATs). Inhibition of OGT via genetic ablation or chemical inhibition improves survival in a medulloblastoma mouse model. These data uncover a critical role for O-GlcNAc signaling in cerebellar development, and pinpoint a potential therapeutic target for Shh-associated medulloblastoma.

2022-06-02 | PXD034270 |

Childhood medulloblastoma

Project description:Childhood medulloblastoma

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Human medulloblastoma ASNSD1 uORF KO LC-MSMS

Project description:A hallmark of high-risk childhood medulloblastoma is the dysregulation of RNA translation. Currently, it is unknown whether medulloblastoma dysregulates the translation of putatively oncogenic non-canonical open reading frames. To address this question, we performed ribosome profiling of 32 medulloblastoma tissues and cell lines and observed widespread non-canonical ORF translation. We then developed a step-wise approach using multiple CRISPR-Cas9 screens to elucidate non-canonical ORFs and putative microproteins implicated in medulloblastoma cell survival. We determined that multiple lncRNA-ORFs and upstream open reading frames (uORFs) exhibited selective functionality independent of the main coding sequence. A microprotein encoded by one of these ORFs, ASNSD1-uORF or ASDURF, was upregulated, associated with the MYC family oncogenes, and was required for medulloblastoma cell survival through engagement with the prefoldin-like chaperone complex. Our findings underscore the fundamental importance of non-canonical ORF translation in medulloblastoma and provide a rationale to include these ORFs in future studies seeking to define new cancer targets.

2024-01-03 | PXD046091 | Pride

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