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Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis

ABSTRACT: Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis

PROVIDER: PRJNA395705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5865490_1.fastq.gz	Fastqsanger.gz
	SRR5865490_2.fastq.gz	Fastqsanger.gz
	SRR5865500_1.fastq.gz	Fastqsanger.gz
	SRR5865500_2.fastq.gz	Fastqsanger.gz
	SRR5865491_1.fastq.gz	Fastqsanger.gz

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Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis (ChIP-seq, RNA-seq)

Project description:Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis (ChIP-seq, RNA-seq)

| PRJNA395707 | ENA

Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis (ChIP-seq, RNA-seq)

Project description:It remains unclear how epigenetic modulators impact the tumorigenic potential of Myc. Here we show that the core subunits, including Dpy30, of the major H3K4 methyltransferase complexes are selectively upregulated in Burkitt lymphoma, and Dpy30 is important for efficient genomic binding of Myc. Dpy30 heterozygosity does not affect normal animal physiology, but significantly suppressed lymphomagenesis and reduced expression of a subset of key pro-survival genes when Myc is hyper-activated. Dpy30 heterozygosity also impedes cellular transformation without affecting normal cell growth. These results suggest that Myc hijacks this chromatin modulator to coordinate its oncogenic program for efficient tumorigenesis, meanwhile creating “epigenetic vulnerability”, which we then exploited by specifically targeting Dpy30’s activity to inhibit growth of the Burkitt lymphoma cell model.

2018-08-01 | GSE101853 | GEO

Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis (Illumina HumanHT-12 V4.0 expression)

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RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication

Project description:RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication

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MYC-driven mouse HCC proteomics

Project description:To identify proteomic signatures associated with hepatocellular carcinoma driven by MYC overexpression, proteomics was performed on the LAP-tTA/tetO-MYC mouse conditional liver cancer model. Upon MYC activation, mice form liver cancer. Differential proteomics was performed in "MYC on" (MYC-HCC) mouse liver tumors versus mouse control normal liver tissue (where MYC was not overexpressed to drive tumorigenesis -- "MYC off").

2022-10-12 | PXD031478 | Pride

Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis

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

2018-08-01 | GSE101854 | GEO

Methionine metabolism and the NOP2 methyltransferase are essential for MYC-Driven liver tumorigenesis

Project description:Hepatocellular carcinoma (HCC) represents the third leading cause of cancer-related death worldwide and has been increasing in recent years in developed nations1,2. The MYC oncogene or its paralogs are frequently amplified or overexpressed in particularly aggressive subtypes of cancer associated with stem cell-like features and worse clinical outcomes3,4, including in liver cancer5. Unfortunately, selective inhibitors that target MYC or its transcriptional program are not yet clinically available for therapy of HCC. Here, we identified methionine metabolism as a selective vulnerability for MYC but not RAS-driven liver cancers. MYC-driven liver cancer cells are methionine dependent and S-adenosylmethionine (SAM), the predominant methyl donor, partially rescues methionine depletion. A low methionine diet, or the methylation inhibitor 5-azacytidine limited MYC-driven tumor formation, but RAS-driven liver cancer was resistant to a low methionine diet. Metabolic tracing of methionine catabolism in MYC high cells identified increased m5C methylation of genomic DNA or ribosomal RNA. We identified NOP2, an rRNA m5C-methyltransferase as a MYC target gene. Knockdown of NOP2 selectively inhibited MYC liver cancer cell proliferation and in vivo tumorigenesis. Thus, methionine catabolism is critical for MYC-driven liver tumorigenesis and NOP2 may serve as a new therapeutic target in liver cancer.

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Specific inhibition of DPY30 activity by peptides suppresses blood cancer cell growth

Project description:Epigenetic modulators are being recognized as attractive targets for potential cancer treatment. SET1/MLL complexes are the major H3K4 methyltransferase complexes in mammals. The DPY30 subunit is associated with these complexes by forming a dimer that directly binds to the ASH2L subunit in the complexes and facilitates methylation. We have previously established an important role of DPY30 in certain hematologic malignancies including MLL-rearranged leukemia and Burkitt’s lymphoma, but the domain on DPY30 that regulates cancer growth is not evident. Moreover, the potential of pharmacologically targeting this chromatin modulator to inhibit cancer has not been explored. Here we have developed a peptide-based strategy to specifically target DPY30 activity. We have designed cell-penetrating peptides that can either bind to DPY30 or show defective or enhanced binding to DPY30. The DPY30-binding peptides, but not the non-binding peptide, inhibit DPY30’s activity in interacting with ASH2L and in enhancing H3K4 methylation. Treatment with the DPY30-binding, but not the non-binding, peptide significantly inhibited the growth of MLL-rearranged leukemia and other MYC-dependent hematologic cancer cells including Burkitt’s lymphoma cells. These results strongly support a critical role of the ASH2L-binding groove of DPY30 in promoting the growth of certain blood cancers, and also demonstrate a proof-of-principle for the feasibility of pharmacologically targeting the ASH2L-binding groove of DPY30 for potential cancer inhibition.

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Project description:Dpy30 regulates Myc binding to targets and Myc-driven tumorigenesis (Illumina HumanHT-12 V4.0 expression)

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Therapeutic targeting nudix hydrolase 1 creates a MYC-driven metabolic vulnerability

Project description:Tumor cells must rewire nucleotide synthesis to satisfy the demands of unbridled proliferation. Meanwhile, they exhibit augmented reactive oxygen species (ROS) production which paradoxically damages DNA and free dNTPs. How these metabolic processes are integrated to fuel tumorigenesis remains to be investigated. MYC family oncoproteins are central regulators that coordinate nucleotide synthesis and ROS generation to drive the development of numerous human cancers. We herein performed a CRISPR-based functional screen targeting metabolic genes and identified nudix hydrolase 1 (NUDT1) as a MYC-driven metabolic dependency. Mechanistically, MYC orchestrated the balance of two metabolic pathways that act in parallel, the NOX4-ROS pathway and the PLK1-NUDT1 nucleotide-sanitizing pathway. We describe LC-1-40 as the first-in-class degrader that potently and selectively depletes NUDT1 in vivo. Administration of LC-1-40 disrupted MYC-controlled metabolic homeostasis, resulting in excessive nucleotide oxidation, cytotoxicity and therapeutic responses in patient-derived xenografts. Thus, pharmacological targeting of NUDT1 represents an actionable MYC-driven metabolic liability.

2023-12-27 | PXD043444 | Pride

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