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RNAseq in Pten enhancer wild-type or deleted mouse T-ALLs

ABSTRACT: RNAseq in Pten enhancer wild-type or deleted mouse T-ALLs

PROVIDER: PRJNA634002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11816559_1.fastq.gz	Fastqsanger.gz
	SRR11816559_2.fastq.gz	Fastqsanger.gz
	SRR11816560_1.fastq.gz	Fastqsanger.gz
	SRR11816560_2.fastq.gz	Fastqsanger.gz
	SRR11816561_1.fastq.gz	Fastqsanger.gz

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RNAseq in Pten enhancer wild-type or deleted mouse T-ALLs

Project description:C57BL6 mice harboring Pten enhancer (PE) conditional knockout NOTCH1-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of PE. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice. GSEA analysis show a significant enrichment of Pten signature genes, consistent with a role of PE in regulating Pten expression.

2020-12-17 | GSE150894 | GEO

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Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO

Project description:To investigate the underlying mechanisms mediating resistance to NOTCH inhibition in Pten-null T-ALL tumor cells we performed gene expression profiling of isogenic Pten-positive and Pten-deleted leukemia lymphoblasts after acute treatment with DBZ in vivo. This analysis revealed that, while direct NOTCH1 target genes (such as Hes1, Dtx1, PtcrA, HeyL and Notch3) are effectively downregulated in both Pten-positive and Pten-deleted tumors, genetic ablation of Pten elicits a global reversal of much of the transcriptional effects of NOTCH inhibition.

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Expression data from isogenic Pten WT or KO mouse T-ALLs treated with DBZ or DMSO

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scRNAseq in Pten enhancer wild-type or deleted thymocytes, enriched for immature thymocyte stages (CD4-CD3-)

Project description:scRNAseq in Pten enhancer wild-type or deleted thymocytes, enriched for immature thymocyte stages (CD4-CD3-)

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scRNAseq in Pten enhancer wild-type or deleted thymocytes, enriched for immature thymocyte stages (CD4-CD3-)

Project description:Single cell suspensions of total thymocytes were obtained from Pten enhancer (PE) wild-type or knockout mice. This single-cell suspension was enriched in CD4-CD3- immature thymocyte progenitor cells. CD4-CD3- enriched thymocytes were then mixed 1:1 with single-cell suspensions from total unenriched thymocytes and subsequntly loaded in a 10x Chromium instrument for single-cell RNAseq analyses. Our results revealed Pten levels are signifcantly decreased in CD4-CD8- double negative (DN) thymocytes, CD8+ intermediate single positive (ISP) thymocytes and CD4+CD8+ double positive (DP) thymocytes in PE knockout mice, compared to PE wild-type mice.

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Project description:C57BL6 mice harboring Sirt1 conditional knockout NOTCH1-HDDPEST-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Sirt1. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice.

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RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

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A Tumor Suppressor Enhancer of PTEN in T-cell development and leukemia

Project description:Long-range oncogenic enhancers play an important role in cancer. Yet, it remains unclear whether similar regulation of tumor suppressor genes is relevant. In this context, loss of expression of the tumor suppressor PTEN is associated with the pathogenesis of various cancers, including T-cell acute lymphoblastic leukemia (T-ALL). Here, we demonstrate that PTEN is regulated in T-cells by a distal enhancer (PE), which is targeted by recurrent focal deletions in T-ALL. This highly conserved regulatory element interacts with and transactivates the PTEN promoter. Consistently, PE deletion in T-ALL cells leads to reduced PTEN levels and proliferative advantage. Moreover, PE-null mice show reduced PTEN levels in the thymus and develop NOTCH1-induced T-ALL with faster kinetics. Furthermore, secondary loss of PE in established leukemias leads to accelerated progression and a gene expression signature driven by Pten loss. Altogether, our results identify PE as the first long-range tumor suppressor enhancer directly implicated in cancer.

2020-12-17 | GSE160427 | GEO

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Project description:Triple transgenic mice harboring a conditional Pten allele were developed and Pten was conditionally deleted in vivo from the lung epithelial cells using the doxycycline dependent Cre/LoxP approach. Microarray analysis of lung RNA isolated from Pten-deleted lung epithelial cells (PtenΔ/Δ) and control mice was performed to identify potential PTEN responsive genes.

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