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PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

ABSTRACT: PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

PROVIDER: PRJNA773061 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16502264_1.fastq.gz	Fastqsanger.gz
	SRR16502264_2.fastq.gz	Fastqsanger.gz
	SRR16502265_1.fastq.gz	Fastqsanger.gz
	SRR16502265_2.fastq.gz	Fastqsanger.gz
	SRR16502266_1.fastq.gz	Fastqsanger.gz

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PRMT7 knockdown in Jurkat-Cas9 and Molt-4 T-ALL cell line

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with only few established prognostic biomarkers.In this study, we examined the expression of protein arginine methyltransferases across hematological malignancies and discovered high levels of PRMT7 mRNA in T-ALL, particularly in the mature subtypes of T-ALL. High PRMT7 was associated with decreased event-free and overall survival in two independent patient cohorts. Genetic deletion of PRMT7 by CRISPR-Cas9 significantly decreased the colony-forming capacity of the cells and negatively impacted cell viability. In the knockout cells, alterations were seen in the monomethyl arginine levels in proteins associated with RNA processing. These results suggest that PRMT7 plays an active role in T-ALL pathogenesis.

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Project description:T cell acute lymphoblastic leukemia (T-ALL) is a hematological malignancy strongly affected by the abnormal activity of transcription factors. Here we report a high expression of developmental transcription factor SIX6 in TAL1 subtype of T-ALL. Our data indicates that this high expression is directly regulated by binding of TAL1 and GATA3 transcription factors into an upstream enhancer element. We also looked into the potential targets of SIX6 in T-ALL and Crispr-cas9 mediated knockout of SIX6 in Jurkat cells caused significant changes in the expression of multiple genes, including genes related to mTOR signaling. In two independent patient cohorts, the high SIX6 expression shows a trend of less favourable prognosis. However, the knockout of SIX6 was not enough to have an effect on proliferation, cell cycle or viability of the Jurkat cells and overexpression of SIX6 in the T-ALL zebrafish model didn’t influence the progression of the disease. Our results show that high expression of SIX6 has a trend towards a less favourable outcome, but SIX6 doesn’t have an independent oncogenic role in T-ALL.

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PRMT7 substrates

Project description:Protein arginine methyltransferases (PRMTs) regulate diverse biological processes and are increasingly being recognized for their potential as drug targets. Here we report the discovery of a potent, selective and cell active chemical probe for PRMT7. SGC3027 is a cell permeable prodrug, which in cells, is converted to SGC8158, a potent, SAM-competitive PRMT7 inhibitor. Inhibition or knockout of cellular PRMT7 resulted in drastically reduced levels of monomethylation of HSP70 family members and other stress-associated proteins. Structural and biochemical analysis revealed that PRMT7-driven in vitro methylation of HSP70 at R469 requires an ATP-bound, open conformation of HSP70. In cells, SGC3027 inhibited methylation of both, constitutive and inducible forms of HSP70, and led to decreased tolerance for perturbations in proteostasis. These results demonstrate a role for PRMT7 in stress response. SGC3027 is the first chemical probe for PRMT7 and together with its inactive control SGC3027N, will be valuable chemical tools to further investigate the role of PRMT7 in human health and disease.

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Transcriptome sequencing of skeletal muscle for PRMT7 knockout mouse

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