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The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer [snRNA-Seq]

ABSTRACT: The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer [snRNA-Seq]

PROVIDER: PRJNA1215436 | ENA |

REPOSITORIES: ENA

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The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

Project description:The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

| PRJNA1158868 | ENA

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer [snRNA-Seq]

Project description:Gene expression profile of STAT-signaling tumor-initiating cells (TIC) in breast xenograft models

2025-01-24 | GSE288006 | GEO

The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer

Project description:Gene expression profile of STAT-signaling tumor-initiating cells (TIC) in breast xenograft models

2024-12-09 | GSE276789 | GEO

hCAF1/CNOT7 regulates interferon signaling by targeting STAT1

Project description:Stringent regulation of the interferon signaling pathway is essential for maintaining the immune response to pathogens and tumors. The transcription factor STAT1 is a crucial mediator of this response. Here we show that hCAF1/CNOT7 regulates class I and II interferon pathways at different crucial steps. In resting cells hCAF1 can control STAT1 trafficking by interacting with the latent form of STAT1 in the cytoplasm. IFN treatment induces STAT1 release, suggesting that hCAF1 may shield cytoplasmic STAT1 from undesirable stimulation. Consistent, hCAF1 silencing enhances STAT1 basal promoter occupancy associated with increased expression of a subset of STAT1-regulated genes. Consequently, hCAF1 knockdown cells exhibit an increased protection against viral infection and reduced viral replication. Furthermore, hCAF1 participates in the extinction of the IFN signal, through its deadenylase activity, by speeding up the degradation of some STAT1-regulated mRNAs. Since abnormal and unbalanced JAK/STAT activation is associated with immune disorders and cancer, hCAF1 could play a major role in innate immunity and oncogenesis, contributing to tumor escape. mRNAs from cells expressing the siRNA siRNA duplexes targeting hCAF1, corresponding to the coding region 941-961 (kd) (hCAF1 NCBI Reference Sequence: NM_013354.5) and one non-targeting control siRNA (mock).

2013-12-31 | E-GEOD-43334 | biostudies-arrayexpress

Interferon-stimulated gene expression in STAT1 knockout cells

Project description:STAT1 plays a cental role in the induction of interferon-stimulated genes, but interferon alpha can activate a STAT1-independent pathway that leads to gene expression. We performed microarray analysis to examine whether like interferon alpha, interferon lambda, a newly discovered interferon, can induce the expression of interferon-stimulated genes in the absence of STAT1. Control and STAT1 knockout Huh-7.5 hepatoma cells were left untreated or treated with 1000 U/ml of human interferon alpha 2a or interferon lambda 1 (PBL) for 24 h, and total RNA was extracted. Sense-strand DNA was generated from 200 ng of total RNA, fragmented, and labeled using a GeneChip WT Plus Reagent Kit (Affymetrix). Six samples were obtained and each sample was anlyzed using one GeneChip.

2016-07-22 | E-GEOD-84693 | biostudies-arrayexpress

hCAF1/CNOT7 regulates interferon signaling by targeting STAT1

2013-12-31 | GSE43334 | GEO

Modified Stat1 Confers Enhanced Interferon Responsiveness and Improved Baseline Antiviral Host Defense

Project description:U3A cells stably expressing wild-type STAT1 or STAT1-CC were treated with interferon beta (10U/ml) or control for 24 hours to assess effects of stat1 modifications, interferon, and the interaction on gene expression. Keywords: interferon, STAT1, STAT1-CC, STAT1CC, STAT-1C, antiviral RNA was isolated from stable U3A-STAT1 lines stably expressing wild-type STAT1 or STAT1CC, after 24 hour treatment with interferon beta (10U/ml) or control.

2015-09-01 | E-GEOD-61413 | biostudies-arrayexpress

Interferon-stimulated gene expression in STAT1 knockout cells

2016-07-22 | GSE84693 | GEO

Modified Stat1 Confers Enhanced Interferon Responsiveness and Improved Baseline Antiviral Host Defense

2015-09-01 | GSE61413 | GEO

Threonine Phosphorylation of STAT1 Restricts Interferon Signaling and Promotes Innate Inflammatory Responses

Project description:Since its discovery over three decades ago, signal transducer and activator of transcription 1 (STAT1) has been extensively studied as a central mediator for interferons (IFNs) signaling and antiviral defense. Here, using genetic and biochemical assays, we unveil Thr748 as a conserved IFN-independent phosphorylation switch in Stat1, which restricts IFN signaling and promotes innate inflammatory responses following the recognition of the bacterial-derived toxin lipopolysaccharide (LPS). Genetically-engineered mice expressing phospho-deficient threonine748–to-alanine (T748A) mutant Stat1 are resistant to LPS–induced lethality. Of note, T748A mice exhibited undisturbed IFN signaling, as well as total expression of Stat1. Further, the T748A point-mutation of Stat1 recapitulates the safeguard effect of the genetic ablation of Stat1 following LPS-induced lethality, indicating that the Thr748 phosphorylation contributes inflammatory functionalities of Stat1. Mechanistically, LPS-induced Toll-like receptor 4 endocytosis activates a cell-intrinsic IκB kinase (IKK)–mediated Thr748 phosphorylation of Stat1, which promotes macrophages inflammatory response while restricting the IFN and anti-inflammatory responses. Depletion of macrophages restores the sensitivity of the T748A mice to LPS-induced lethality. Together, our study indicates a phosphorylation-dependent functional dichotomy of Stat1 in innate immune responses: IFN phospho-tyrosine dependent, and inflammatory phospho-threonine dependent. Better understanding of the Thr748 phosphorylation of Stat1 may uncover novel pharmacologically targetable molecules and offer better treatment modalities for sepsis, a disease that claims millions of lives annually.

2024-03-18 | GSE261824 | GEO

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