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NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [RNA-seq]

ABSTRACT: NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [RNA-seq]

PROVIDER: PRJNA1026472 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26332729_1.fastq.gz	Fastqsanger.gz
	SRR26332729_2.fastq.gz	Fastqsanger.gz
	SRR26332730_1.fastq.gz	Fastqsanger.gz
	SRR26332730_2.fastq.gz	Fastqsanger.gz
	SRR26332731_1.fastq.gz	Fastqsanger.gz

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NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING

Project description:NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING

| PRJNA1026467 | ENA

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [scRNA-seq]

Project description:NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [scRNA-seq]

| PRJNA1026474 | ENA

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [CHIP-seq]

Project description:NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [CHIP-seq]

| PRJNA1026473 | ENA

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [RNA-seq]

Project description:Downregulation of antigen presentation and lack of immune infiltration are defining features of small cell lung cancer (SCLC) limiting response to immune checkpoint blockade (ICB), While a high MHC Class I, immune-inflamed subset benefits from ICB, underlying mechanisms of immune response in SCLC have yet to be elucidated. Here we show that in the landmark IMpower133 clinical trial high, but not low, NOTCH1 expression is significantly associated with longer survival with the addition of ICB to chemotherapy among ~80% of SCLC patients with neuroendocrine-enriched tumors (ASCL1-enriched, HR 0.39, P=0.0012; NEUROD1-enriched, HR 0.44, P=0.024). Genetic or pharmacologic activation of NOTCH1 in ASCL1 and NEUROD1 SCLC cell lines dramatically up-regulates MHC Class I through epigenetic up-regulation of STING. In syngeneic mouse models, Notch1 activation reprograms SCLC tumors from immune-excluded to immune-inflamed, facilitating durable, complete responses with ICB combined with a STING agonist. STING1 expression is significantly enriched in high compared to low NOTCH1 expressing tumors in IMpower133 thereby validating our proposed mechanism. Our data reveal a previously undiscovered role for NOTCH1 as a critical driver of SCLC immunogenicity and a potential predictive biomarker for ICB in SCLC. NOTCH1 activation may be a therapeutic strategy to unleash anti-tumor immune responses in SCLC and other neuroendocrine cancers in which NOTCH1 is typically suppressed.

2025-06-02 | GSE244945 | GEO

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [CHIP-seq]

2025-06-02 | GSE244944 | GEO

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING [scRNA-seq]

2025-06-22 | GSE244946 | GEO

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING.

Project description: Not available

| S-EPMC12435836 | biostudies-literature

NOTCH1 reverses immune suppression in small cell lung cancer through reactivation of STING

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-06-04 | GSE244947 | GEO

STING suppresses the reactivation of dormant metastasis

Project description:STING suppresses the reactivation of dormant metastasis

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Barrier-to-autointegration Factor 1 (BAF) Promotes Gammaherpesvirus Reactivation from Latency

Project description:Gammaherpesviruses, including Kaposi’s sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV), are DNA viruses that are globally associated with human cancers and establish lifelong latency in the human population. Detection of gammaherpesviral infection by the cGAS-STING innate immune DNA-sensing pathway is critical for suppressing viral reactivation from latency, a process that promotes viral pathogenesis and transmission. We report that Barrier-to-autointegration factor 1 (BAF)-mediated suppression of the cGAS-STING signaling pathway is necessary for reactivation of KSHV and EBV. We demonstrate a novel role for BAF in destabilizing cGAS expression and show that BAF expression in latently infected, reactivating, or uninfected cells leads to suppression of type I interferon-mediated antiviral responses and inhibition of viral replication. Furthermore, BAF overexpression resulted in decreased cGAS expression at the protein level. These results establish BAF as a key regulator of the lifecycle of gammaherpesviruses and a potential target for treating viral infections and malignancies.

2022-12-12 | GSE200781 | GEO

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