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The SUMO Pathway as a Therapeutic Option in Pancreatic Cancer

ABSTRACT: The SUMO Pathway as a Therapeutic Option in Pancreatic Cancer

PROVIDER: PRJNA489233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7782590.fastq.gz	Fastqsanger.gz
	SRR7782591.fastq.gz	Fastqsanger.gz
	SRR7782592.fastq.gz	Fastqsanger.gz
	SRR7782587.fastq.gz	Fastqsanger.gz
	SRR7782588.fastq.gz	Fastqsanger.gz

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The SUMO Pathway as a Therapeutic Option in Pancreatic Cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with overall five-year survival of 8%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC, however subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumor biology. It is clear that hyperactivation of MYC generates dependencies, which can be exploited therapeutically. To find MYC-associated dependency we analyzed human PDAC expression dataset. We observed that MYC is connected to the sumoylation machinery in PDAC. Components of the SUMO pathway mark a PDAC subtype with worse prognosis and we provide evidence that PDACs with a MYChigh/SUMOhigh phenotype respond to a novel SUMO inhibitor, offering the opportunity to develop novel stratified PDAC therapies

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Project description:The SUMO Pathway as a Therapeutic Option in Pancreatic Cancer

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Project description:Ribosomal RNAs (rRNAs) are essential components of the ribosome and are among the most abundant macromolecules in the cell. To ensure high rRNA level, eukaryotic genomes contain dozens to hundreds of rDNA genes, however, only a fraction of the rRNA genes seems to be active, while others are transcriptionally silent. In Drosophila rDNA units damaged by insertions of retrotransposons are repressed by an unknown mechanism. Here, we established a new model to study regulation of rDNA expression using molecularly marked rDNA transgenes. Using this model, we show that insertion of any heterologous sequence into rDNA leads to transcriptional repression. We found that SUMO (Small Ubiquitin-like Modifier) is required for efficient repression of damaged rDNA units. Surprisingly, SUMO also controls expression of intact rDNA, demonstrating that a single pathway is responsible for both selective repression of damaged units and silencing of surplus rDNA.

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