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Unrestricted SUMOylation drives lymphomagenesis

ABSTRACT: Unrestricted SUMOylation drives lymphomagenesis

PROVIDER: PRJNA595164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10677187.fastq.gz	Fastqsanger.gz
	SRR10677188.fastq.gz	Fastqsanger.gz
	SRR10677189.fastq.gz	Fastqsanger.gz
	SRR10677190.fastq.gz	Fastqsanger.gz
	SRR10677191.fastq.gz	Fastqsanger.gz

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Unrestricted SUMOylation drives lymphomagenesis

Project description:Unrestricted SUMOylation drives lymphomagenesis

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Actionable loss of SLF2 drives B-cell lymphomagenesis and impairs the DNA damage Response

Project description:The DNA damage response (DDR) acts as a barrier to malignant transformation and is often impaired during tumorigenesis. Exploiting the impaired DDR can be a promising therapeutic strategy; however, the mechanisms of inactivation and corresponding biomarkers are incompletely understood. Starting from an unbiased screening approach, we identified the SMC5-SMC6 Complex Localization Factor 2 (SLF2) as a regulator of the DDR and biomarker for a B-cell lymphoma (BCL) patient subgroup with an adverse prognosis. SLF2-deficiency leads to loss of DDR factors including CLSPN and consequently impairs CHK1 activation. In line with this mechanism, genetic deletion of Slf2 drives lymphomagenesis in vivo. Tumor cells lacking SLF2 are characterized by a high level of DNA damage, which leads to alterations of the post-translational SUMOylation pathway as a safeguard. The resulting co-dependency confers synthetic lethality to a clinically applicable SUMOylation inhibitor (SUMOi), and inhibitors of the DDR pathway act highly synergistic with SUMOi. Together, our results identify SLF2 as a DDR regulator and reveal co-targeting of the DDR and SUMOylation as a promising strategy for the treatment of aggressive lymphoma.

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Actionable loss of SLF2 drives B-cell lymphomagenesis and impairs the DNA damage Response

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Actionable genetic alterations of the SUMO isopeptidase SENP6 drive lymphomagenesis and genetic instability in diffuse large B-cell lymphoma

Project description:SUMOylation is a post-translational modification of proteins that regulates these proteins’ localization, turnover or function. Aberrant SUMOylation is frequently found in cancers but its origin remains elusive. Using a genome-wide transposon mutagenesis screen in a MYC-driven B-cell lymphoma model, we identified the SUMO isopeptidase (or deconjugase) SENP6 as a tumor suppressor that links unrestricted SUMOylation to tumor development and progression. Notably, SENP6 is recurrently deleted in human lymphomas and SENP6 deficiency results in unrestricted SUMOylation. Mechanistically, SENP6 loss triggers release of DNA repair- and genome maintenance-associated protein complexes from chromatin thereby impairing DNA repair in response to DNA damages and ultimately promoting genomic instability. In line with this hypothesis, SENP6 deficiency drives synthetic lethality to PARP inhibition. Together, our results link SENP6 loss to defective genome maintenance and reveal the potential therapeutic application of PARP inhibitors in B-cell lymphoma.

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Histone 1 deficiency drives lymphomagenesis through disruption of 3D chromatin architecture

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A SUMOylation-induced Satb1/Satb2 switch drives embryonic stem cell differentiation

Project description:A SUMOylation-induced Satb1/Satb2 switch drives embryonic stem cell differentiation

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A SUMOylation-induced Satb1/Satb2 switch drives embryonic stem cell differentiation [HiC]

Project description:A SUMOylation-induced Satb1/Satb2 switch drives embryonic stem cell differentiation [HiC]

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hpr1 sumoylation mutant

Project description:To gain insight into the impact of THO complex sumoylation on gene expression in yeast S. cerevisiae, total RNAs were extracted from wt and hpr1-KR cells and transcriptome profiles were analyzed by Agilent microarrays. The hpr1 K-R mutant is a version of the hpr1 THO subunit in which lysines 60-65 were simultaneously mutated, which abrogated the sumoylation of the protein.

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SUMOylation of Linker Histone H1 Drives Chromatin Condensation and Restriction of Embryonic Cell Fate Identity [ChIP-seq]

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