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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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SIX6 knockdown in Jurkat-Cas9 T-ALL cell line

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SIX6 knockdown in Jurkat-Cas9 T-ALL cell line

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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Transcriptome analysis of Jurkat T-ALL clones from control and CBAP-knockdown/knockout sets

Project description:We sequenced whole-genome mRNA from 8 different single stable clones of Jurkat cells modified with CBAP gene expression usng shRNA knockdown or CRISPR/Cas9-mediated knockout and their controls.

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Project description:To explore the mechanism by which PRMT7 regulates HCC cell malignant phenotypes, we performed RNA-seq in QGY-7703 cells before and after PRMT7 knockdown to identify the affected signaling pathways. 296 differentially expressed genes were identified in PRMT7-downregulated cells (Figure 6A) and these genes were enriched in cancer-related pathways including MAPK signaling pathway, p53 signaling pathway, and FoxO signaling pathway (Figure 6B), as revealed by DAVID KEGG analysis.

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MS-based arginine monomethylation study in Jurkat PRMT7 KO cells

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Transcription profiling by array of human Jurkat T cells either over-expressing miR-146a or with miR-146a knockdown

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