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Gene expression difference between normal and Pten-deficient 5-HT neurons

ABSTRACT: Gene expression difference between normal and Pten-deficient 5-HT neurons

PROVIDER: PRJNA691327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13404673.fastq.gz	Fastqsanger.gz
	SRR13404673_1.fastq.gz	Fastqsanger.gz
	SRR13404673_2.fastq.gz	Fastqsanger.gz
	SRR13404674.fastq.gz	Fastqsanger.gz
	SRR13404674_1.fastq.gz	Fastqsanger.gz

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Gene expression difference between normal and Pten-deficient 5-HT neurons

Project description:Purpose: compare the gene expression diffenrence between wildtype and Pten-deficient 5-HT neurons. Methods: 5-HT neurons cell body are collected from acut brain slice with patch electrodes. Pten-deficient 5-HT neurons are obtained from Pet1-Cre; Ptenflox/flox mice. Normal 5-HT neurons are obtained from littermate wildtype mice. Reverse transcription was performed using a SMARTer Ultra Low RNA Kit (Clontech, Japan). Single-cell cDNA was amplified using an Advantage 2 PCR Kit (Clontech, Japan). Purified cDNA from individual cells were sequenced using the Illumina HiSeq 2000 platform. Sequence reads were aligned to the mouse mm9 genome using TopHat. Differential expression analysis was performed using DESeq (Bioconductor) followed by Student t-test. Genes were considered differentially expressed if p<0.05. Results: The somatic compartments of individual YFP-labeled 5-HT neurons in acute brain slices were harvested for RNA sequencing. Each of the cells had 2 X 107 reads mapping back to the mouse genome when analyzed using the RUM mapping program. We found 859 genes (381 up-regulated, 478 down-regulated) were differentially expressed in Pten-deficient 5-HT neurons. Gene ontology of differentially expressed genes revealed the biological processes up-regulated and down-regulated in Pten-deficient 5-HT neurons. The absence of Pten in 5-HT neurons was associated with significantly increased expression of genes involved in the regulation of axonal extension and cell size, cell morphogenesis and cytoskeleton organization

2021-01-12 | GSE164610 | GEO

Synthetic essentiality of metabolic regulator PDHK1 in PTEN-deficient cells and cancer

Project description:PTEN is a tumor suppressor that is often inactivated in cancer and possesses both lipid and protein phosphatase activities. We report the metabolic regulator PDHK1 (pyruvate dehydrogenase kinase1) is a synthetic-essential gene in PTEN-deficient cancer and normal cells. The predominant mechanism of PDHK1 regulation and dependency is the PTEN protein phosphatase dephosphorylates NFkB activating protein (NKAP) and limits NFkB activation to suppress expression of PDHK1, a NFkB target gene. Loss of the PTEN protein phosphatase upregulates PDHK1 to drive aerobic glycolysis and induce PDHK1 cellular dependence. PTEN-deficient human tumors harbor increased PDHK1, which is a biomarker of decreased patient survival, establishing clinical relevance. This study uncovers a PTEN-regulated signaling pathway and reveals PDHK1 as a potential target in PTEN-deficient cancers.

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Expression data of PTEN deficient PKO cells

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miRNA expression in PTEN-deficient premalignant DP thymocytes

Project description:T cell-specific deletion of PTEN induces premalignancy in CD4+ CD8+ (DP) immature T cells in the thymus, which progresses to the development of mature CD4+ T cell lymphomas in the lymph nodes and spleen. As part of a screen to identify factors that inhibit progression to malignancy, we compared miRNA expression in premalignant PTEN-deficient DP thymocytes versus wild-type controls. DP thymocytes were collected by cell sorting from three 9-week-old, premalignant T cell-specific PTEN-deficient mice (tPTEN-/-) and three littermate controls. miRNA expression was assessed relative to a reference pool generated from an equal mixture of all samples.

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PI3Kβ controls immune evasion in PTEN-deficient breast tumors

Project description:Loss of the PTEN tumor suppressor is one of the most common oncogenic drivers across all cancer types. PTEN is the major negative regulator of phosphoinositide-3 kinase (PI3K) signaling. Notably, the PI3Kβ isoform has been shown to play an important role in PTEN-deficient tumors, but the mechanisms underlying the importance of PI3Kβ activity remain elusive. Using a syngeneic genetically-engineered mouse (GEM) model of invasive breast cancer driven by concurrent ablation of Pten and Trp53 (p53), we showed that genetic inactivation of PI3Kβ led to a robust anti-tumor immune response that abrogated tumor growth in syngeneic immunocompetent mice, but not in immunodeficient mice. Mechanistically, PI3Kβ inactivation in the PTEN-null setting led to reduced STAT3 signaling and increased expression of immune stimulatory molecules, thereby promoting anti-tumor immune responses. Pharmacological PI3Kβ inhibition also elicited anti-tumor immunity, and synergized with immunotherapy to inhibit tumor growth. Mice with complete responses to the combined treatment displayed immune memory and rejected tumors upon re-challenge. Our findings demonstrate a molecular mechanism linking PTEN loss and STAT3 activation in cancer and suggest that PI3Kβ controls immune escape in PTEN-null tumors, providing a rationale for combining PI3Kβ inhibitors with immunotherapy for the treatment of PTEN-deficient breast cancer.

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miRNA expression in PTEN-deficient premalignant DP thymocytes

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sequencing data from control and PTEN-deficient mouse brain microvascular transcriptomes

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Yap1 ChIP-seq in Pten/Smad4-deficient mouse prostate cancer cells

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PI3Kβ controls immune evasion in PTEN-deficient breast tumors

Project description:PI3Kβ controls immune evasion in PTEN-deficient breast tumors

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PI3Kβ controls immune evasion in PTEN-deficient breast tumors

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