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SHQ1 regulation of RNA splicing is required for T-lymphoblastic leukemia cell survival

ABSTRACT: SHQ1 regulation of RNA splicing is required for T-lymphoblastic leukemia cell survival

PROVIDER: PRJNA481581 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7533580_1.fastq.gz	Fastqsanger.gz
	SRR7533580_2.fastq.gz	Fastqsanger.gz
	SRR7533581_1.fastq.gz	Fastqsanger.gz
	SRR7533581_2.fastq.gz	Fastqsanger.gz
	SRR7533582_1.fastq.gz	Fastqsanger.gz

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SHQ1 regulation of RNA splicing is required for T-lymphoblastic leukemia cell survival

Project description:T-acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy with complicated heterogeneity. Although expression profiling reveals common elevated genes in distinct T-ALL subtypes, little is known about their functional role(s) and regulatory mechanism(s). We here show the expression of SHQ1, an H/ACA snoRNPs assembly factor involved in snRNA pseudouridylation, is specifically and highly expressed in T-ALL. Mechanistically, oncogenic NOTCH1 directly binds to the SHQ1 promoter and activates its transcription. SHQ1 depletion induces massive leukemia cell death in vitro and in vivo, and prolongs animal survival in murine T-ALL models. RNA-Seq reveals that SHQ1 depletion impairs widespread RNA splicing, and MYC is one of the most prominently downregulated genes due to inefficient splicing. Ectopically expressed MYC significantly rescues T-ALL cell death resulted from SHQ1 inactivation. We herein report a previously unsuspected mechanism of NOTCH1-SHQ1-MYC axis in T cell leukemogenesis. Our findings not only shed light on the role of SHQ1 in promoting RNA splicing and tumorigenesis, but also provide a new mechanism of MYC regulation.

2018-10-23 | GSE117264 | GEO

Characterization of co-transcriptional splicing in acute lymphoblastic leukemia

Project description:Alternative splicing is a promising therapeutic target in acute lymphoblastic leukemia. Here, we report the alternative splicing changes in B-ALL cell lines including NALM6 cells and MUTZ-5 cells treated with DYRK1 inhibitor, EHT 1610 and GNF 2133. Dysregulation of co-transcriptional splicing is a therapeutic target in acute lymphoblastic leukemia (ALL). Here, we detected the alternative splicing in NALM6 cells or MUTZ-5 cells treated with EHT 1610 or GNF2133. We detected the alternative splicing in NALM6 cells cells treated with THAL-SNS-032. We also determined the alternative splicing in MEF2D-BCL9 ALL and MEF2D-HNRNPUL1 ALL patient xenografted samples treated with E7820, a anticancer sulfamide, or DMSO. Furthermore, ChIP-seq for RNA polymerase II (Pol II), p-Ser2 Pol II, and p-Ser5 Pol II were performed after DMSO or EHT 1610 treatment in NALM6 cells. ChIP-seq for p-Ser2 Pol II, and p-Ser5 Pol II were performed after DMSO or THAL-SNS-032 treatment in NALM6 cells.PRO-seq in NALM6 cells treated with DMSO, EHT 1610, and THAL-SNS-032 were performed.

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The Splicing Factor PTBP1 Interacts with RUNX1 and is Required for Leukemia Cell Survival [CUT&Tag]

Project description:The Splicing Factor PTBP1 Interacts with RUNX1 and is Required for Leukemia Cell Survival [CUT&Tag]

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The Splicing Factor PTBP1 Interacts with RUNX1 and is Required for Leukemia Cell Survival [Long Read]

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The Splicing Factor PTBP1 Interacts with RUNX1 and is Required for Leukemia Cell Survival [Long Read]

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