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Epigenetic silencing of STAT3-targeted miR-193a, by constitutive activation of JAK/STAT signaling, leads to tumor progression through overexpression of YWHAZ in gastric cancer

ABSTRACT: To investigate aberrant JAK/STAT signalling conferred epigenetic silencing of miR-193a, leading to overexpression of YWHAZ and metastasis in gastric cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE154080 | GEO | 2021/02/24

REPOSITORIES: GEO

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Epigenetic silencing of STAT3-targeted miR-193a, by constitutive activation of JAK/STAT signaling, leads to tumor progression through overexpression of YWHAZ in gastric cancer

Project description:Epigenetic silencing of STAT3-targeted miR-193a, by constitutive activation of JAK/STAT signaling, leads to tumor progression through overexpression of YWHAZ in gastric cancer

| PRJNA645079 | ENA

Epigenetic Silencing of STAT3-Targeted miR-193a, by Constitutive Activation of JAK/STAT Signaling, Leads to Tumor Progression Through Overexpression of YWHAZ in Gastric Cancer.

Project description: Not available

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JAK/STAT blockade in cHL

Project description:Here we investigated the effects of JAK/STAT pharmacological inhibition on cHL cell models using ruxolitinib, a JAK 1/2 inhibitor. We use five classical Hodgkin lymphoma cell lines: L428, L1236, L540, KMH2, L591

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JAK-STAT pathways maintain homeostasis in immune cells (ATAC-Seq)

Project description:Immune cells need to sustain a state of constant alertness over a lifetime. Yet, little is known about the regulatory processes that control the fluent and fragile balance that is called homeostasis. Here we demonstrate that JAK-STAT signaling, beyond its role in immune responses, is a major regulator of immune cell homeostasis. We investigated JAK-STAT-mediated transcription and chromatin accessibility across 12 mouse models, including knockouts of all STAT transcription factors and of the TYK2 kinase. Baseline JAK-STAT signaling was detected in CD8+ T cells and macrophages of unperturbed mice – but abrogated in the knockouts and in unstimulated immune cells deprived of their normal tissue context. We observed diverse transcription-regulatory programs, including gene regulation by STAT2 and IRF9 independent of STAT1. In summary, our large-scale dataset and integrative analysis of JAK-STAT mutant and wildtype mice uncovered a crucial role of JAK-STAT signaling in unstimulated immune cells, where it contributes to a poised epigenetic and transcription-regulatory state and helps prepare these cells for rapid response to immune stimuli.

2024-02-24 | GSE204734 | GEO

Somatic IL4R Hotspot Mutations in Primary Mediastinal Large B-cell lymphoma lead to constitutive JAK-STAT activation

Project description:Primary mediastinal large B cell lymphoma (PMBCL) is a distinct subtype of diffuse large B cell lymphoma thought to arise from thymic medullary B cells. Gene mutations underlying the molecular pathogenesis of the disease are incompletely characterized. Here, we describe novel somatic IL4R mutations in 15 out of 62 primary cases of PMBCL (24.2%) and in all PMBCL-derived cell lines tested. The majority of mutations (11/21; 52%) were hotspot single nucleotide variants in exon 8 leading to an I242N amino acid change in the transmembrane domain. Functional analyses establish this mutation as gain-of-function leading to constitutive activation of the JAK-STAT pathway and upregulation of downstream cytokine expression profiles and B cell specific antigens. Moreover, expression of I242N mutant IL4R in a mouse xenotransplantation model conferred growth advantage in vivo. The pattern of concurrent mutations within the JAK-STAT signaling pathway suggests additive/synergistic effects of these gene mutations contributing to lymphomagenesis. Our data establish IL4R mutations as novel driver alterations and provide a strong preclinical rationale for therapeutic targeting of JAK-STAT signaling in PMBCL.

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Targets of JAK STAT signaling in Drosophila cells

Project description:Purpose: analyze ligand and receptor genes regulated at early time points following JAK STAT pathway stimulation During development and homeostasis, cells integrate multiple signals originating either from neighboring cells or systemically. In turn, responding cells can produce signals that act in an autocrine, paracrine, or endocrine manner. Although the nature of the signals and pathways used in cell-cell communication are well characterized, we lack, in most cases, an integrative view of signaling describing the spatial and temporal interactions between pathways (e.g., whether the signals are processed sequentially or concomitantly when two pathways are required for a specific outcome). To address the extent of cross-talk between the major metazoan signaling pathways, we characterized immediate transcriptional responses to either single- or multiple pathway stimulations in homogeneous Drosophila cell lines. Our study, focusing on seven core pathways, epidermal growth factor receptor (EGFR), bone morphogenetic protein (BMP), Jun kinase (JNK), JAK/STAT, Notch, Insulin, and Wnt, revealed that many ligands and receptors are primary targets of signaling pathways, highlighting that transcriptional regulation of genes encoding pathway components is a major level of signaling cross-talk. In addition, we found that ligands and receptors can integrate multiple pathway activities and adjust their transcriptional responses accordingly. RNA-seq data is for JAK STAT pathway only

2018-12-01 | GSE123167 | GEO

JAK-STAT signaling maintains homeostasis in T cells and macrophages (RNA-seq)

2024-02-24 | GSE204735 | GEO

JAK-STAT signaling maintains homeostasis in T cells and macrophages (spatial transcriptomics)

2024-02-24 | GSE227168 | GEO

Jak/Stat3 regulated global gene expression dynamics during late-stage reprogramming process

Project description:We performed RNAseq analysis to dissect the dynamic transcriptome change during mouse iPSC induction, with or without blocking the Jak/Stat3 activity. We described Jak/Stat3 activity-specific global gene expression patterns, biological events, and regulation of key pluripotent genes, epigenetic modulators, and non-coding RNAs during the reprogramming process. We further demonstrated that Jak/Stat3 activity is essential for proper imprint of Dlk1-Dio3 region that is necessary for complete pluripotency establishment. Functional analysis revealed that one Jak/Stat3 downstream targets identified in our study - Esrrb significantly rescues reprogramming despite the inhibition of Jak/Stat3 activity. Our data illustrated novel mechanism in Jak/Stat3 promoted pluripotency establishment, which is valuable for further improvement of naïve-state iPSC generation across different species.

2017-08-18 | GSE97261 | GEO

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