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STING suppresses the reactivation of dormant metastasis

ABSTRACT: STING suppresses the reactivation of dormant metastasis

PROVIDER: PRJNA868358 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21007473_1.fastq.gz	Fastqsanger.gz
	SRR21007473_2.fastq.gz	Fastqsanger.gz
	SRR21007474_1.fastq.gz	Fastqsanger.gz
	SRR21007474_2.fastq.gz	Fastqsanger.gz
	SRR21007475_1.fastq.gz	Fastqsanger.gz

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STING suppresses the reactivation of dormant metastasis

Project description:Metastatic relapse frequently develops from disseminated cancer cells that remain dormant in distant organs after the apparently successful treatment of a primary tumor. Disseminated cancer cells fluctuate between immune evasive quiescent and cell cycle reentry states, which exposes them to elimination by the immune system. Little is known about the molecules that determine immune-mediated clearing of awakened metastatic cells and how this process could be therapeutically activated to eliminate residual disseminated disease in patients. Here, we use models of indolent metastasis to identify cancer cell-intrinsic determinants of immune reactivity during cancer cell exit from dormancy. Through in vivo genetic screens of tumor-intrinsic immune regulators, we identified the STING (stimulator of interferon genes) pathway as a suppressor of metastatic outbreak in dormant models of human and mouse lung adenocarcinoma metastasis. STING levels and signaling activity rise in metastatic progenitors that reenter the cell cycle and are dampened by STING enhancer hypermethylation in breakthrough metastases or enhancer chromatin repression in cells reentering dormancy in response to TGF-β. STING expression in cancer cells from spontaneous metastases suppresses their outgrowth in a NK cell- and CD8+ T cell-dependent manner. Systemic treatment of mice with pharmacologic STING agonists eliminates indolent metastatic cells and prevents spontaneous metastasis, both effects requiring cancer cell STING function. Thus, STING signaling represents a checkpoint against the progression of dormant metastasis and suggests a therapeutically actionable strategy for the prevention of disease relapse. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modification markers H3K4me1, H3K4me3, H3K27ac in human lung cancer cells at different stages of metastasis and in cells treated with TGF-β or not.

2023-01-30 | GSE210946 | GEO

Project description:STING suppresses the reactivation of dormant metastasis

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Project description:STING suppresses the reactivation of dormant metastasis

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Project description:STING suppresses the reactivation of dormant metastasis

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STING inhibits the reactivation of dormant metastasis in lung adenocarcinoma.

Project description:Metastasis frequently develops from disseminated cancer cells that remain dormant after the apparently successful treatment of a primary tumour. These cells fluctuate between an immune-evasive quiescent state and a proliferative state liable to immune-mediated elimination1-6. Little is known about the clearing of reawakened metastatic cells and how this process could be therapeutically activated to eliminate residual disease in patients. Here we use models of indolent lung adenocarcinoma metastasis to identify cancer cell-intrinsic determinants of immune reactivity during exit from dormancy. Genetic screens of tumour-intrinsic immune regulators identified the stimulator of interferon genes (STING) pathway as a suppressor of metastatic outbreak. STING activity increases in metastatic progenitors that re-enter the cell cycle and is dampened by hypermethylation of the STING promoter and enhancer in breakthrough metastases or by chromatin repression in cells re-entering dormancy in response to TGFβ. STING expression in cancer cells derived from spontaneous metastases suppresses their outgrowth. Systemic treatment of mice with STING agonists eliminates dormant metastasis and prevents spontaneous outbreaks in a T cell- and natural killer cell-dependent manner-these effects require cancer cell STING function. Thus, STING provides a checkpoint against the progression of dormant metastasis and a therapeutically actionable strategy for the prevention of disease relapse.

| S-EPMC10569211 | biostudies-literature

Glutamine supplementation suppresses herpes simplex virus reactivation

Project description:Glutamine supplementation suppresses herpes simplex virus reactivation

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TGF-β protects dormant metastasis from immune mechanosurveillance

Project description:TGF-β protects dormant metastasis from immune mechanosurveillance

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C9orf72 in myeloid cells suppresses STING-induced inflammation

Project description:C9orf72 in myeloid cells suppresses STING-induced inflammation

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PRSS8 Suppresses Colorectal Carcinogenesis and Metastasis.

Project description:PRSS8 Suppresses Colorectal Carcinogenesis and Metastasis.

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Profiling the proteome of Mycobacterium tuberculosis during dormancy and reactivation

Project description:Tuberculosis, caused by Mycobacterium tuberculosis, still remains a major global health problem. The main obstacle in eradicating this disease is the ability of this pathogen to remain dormant in macrophages, and to get reactivated later under immuno-compromised conditions. The physiology of hypoxic nonreplicating M. tuberculosis is well studied using many in vitro dormancy models. However, the physiological changes that take place during the shift from dormancy to aerobic growth (reactivation) have rarely been subjected to a detailed investigation. In this study, we developed an in vitro reactivation system by re-aerating bacteria that were made dormant employing Wayne’s dormancy model, and compared the proteome profiles of dormant and reactivated bacteria using label-free one-dimensional LC/MS/MS analysis.

2015-06-01 | PXD001158 | Pride

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