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STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE297764 | GEO | 2025/12/02

REPOSITORIES: GEO

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STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways

Project description:Meningiomas are common tumors of the central nervous system that are typically treated with surgery but lack alternative treatment options. Activation of the stimulator of interferon genes pathway with an agonist such as 8803 can trigger anti-tumor immune responses. Using integrated molecular approaches, here we show this pathway is expressed in both neoplastic and immune populations within meningiomas associated with promoter hypomethylation and increased chromatin accessibility. Treatment of diverse patient meningiomas ex vivo with 8803 induces direct tumor cytotoxicity through pyroptosis and the induction of gasdermin D membrane pore formation. Direct tumor cytotoxicity triggered by 8803 activates macrophages and upregulates matrix metalloproteinase production facilitating degradation of tumor stroma collagen. Treatment of preclinical meningiomas with 8803 induces survival benefits, including in an immune competent orthotopic setting, through remodeling of the tumor microenvironment, immune infiltration, and down regulation of tumor-mediated immune suppression thereby nominating 8803 for treatment consideration in meningiomas.

2025-12-02 | GSE297637 | GEO

STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways [scRNA-Seq]

2026-03-26 | GSE323014 | GEO

STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways [scMulti-omics]

2025-12-02 | GSE297758 | GEO

STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways

Project description:STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways

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STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways

Project description:STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways

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STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways [scRNA-Seq]

Project description:STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways [scRNA-Seq]

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STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways [scMulti-omics]

Project description:STING activation induces cytotoxic and immune responses in meningiomas via inflammatory cell death pathways [scMulti-omics]

| PRJNA1266132 | ENA

Cutting Edge: Activation of STING in T Cells Induces Type I IFN Responses and Cell Death.

Project description:Stimulator of interferon genes (STING) was initially described as a sensor of intracellular bacterial and viral DNA and a promising adjuvant target in innate immune cells; more recently STING has also been shown to detect endogenous DNA and play a role in tumor immunity and autoimmune disease development. Thus far STING has been studied in macrophages and dendritic cells. In this study, to our knowledge we provide the first evidence of STING activation in T cells, in which STING agonists not only provoke type I IFN production and IFN-stimulated gene expression, mirroring the response of innate cells, but are also capable of activating cell stress and death pathways. Our results suggest a re-evaluation of STING agonist-based therapies may be necessary to identify the possible effects on the T cell compartment. Conversely, the effects of STING on T cells could potentially be harnessed for therapeutic applications.

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Thrombin induces morphological and inflammatory astrocytic responses via activation of PAR1 receptor.

Project description:Spinal cord injury (SCI) will result in the significant elevation of thrombin production at lesion site via either breakage of blood-spinal cord barrier or upregulated expression within nerve cells. Thrombin-induced activation of the protease activated receptors (PARs) evokes various pathological effects that deteriorate the functional outcomes of the injured cord. The cellular consequences of thrombin action on the astrocytes, as well as the underlying mechanism are not fully elucidated by far. In the present study, SCI model of rats was established by contusion, and primary astrocytes were isolated for culture from newborn rats. The expression levels of thrombin and PAR1 receptor at lesion sites of the spinal cord were determined. The primary astrocytes cultured in vitro were stimulated with different concentration of thrombin, and the resultant morphological changes, inflammatory astrocytic responses, as well as PAR1-activated signal pathway of astrocytes were accordingly examined using various agonists or antagonists of the receptor. Thrombin was found to reverse astrocytic stellation, promote proliferation but inhibit migration of astrocytes. Furthermore, the serine protease was shown to facilitate inflammatory response of astrocytes through regulation of MAPKs/NFκB pathway. Our results have provided the morphological evidence of astrocytic reactivity in response to thrombin stimulation and its neuroinflammatory effects following SCI, which will be indicative for the fundamental insights of thrombin-induced neuropathology.

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Honokiol induces paraptosis-like cell death of acute promyelocytic leukemia via mTOR & MAPK signaling pathways activation.

Project description:Acute promyelocytic leukemia (APL) is a blood system disease caused by the accumulation of a large number of immature blood cells in bone marrow. Although the introduction of all-trans retinoic acid (ATRA) and arsenic has reached a high level of complete remission rate and 5-year disease-free survival rate, the occurrence of various adverse reactions still severely affects the quality of life of patients. As a natural product, honokiol (HNK) has the advantages of low toxicity and high efficiency, and it is a potential drug for the treatment of cancer. Since cancer cells can escape apoptotic cell death through multiple adaptive mechanisms, HNK, a drug that induces cancer cell death in a nonapoptotic way, has attracted much interest. We found that HNK reduced the viability of human APL cell line (NB4 cells) by inducing paraptosis-like cell death. The process was accompanied by excessive reactive oxygen species (ROS), mitochondrial damage, endoplasmic reticulum stress, and increased microtubule-associated protein 1 light chain 3 (LC3) processing. The inactivation of proteasome activity was the main cause of misfolded and unfolded protein accumulation in endoplasmic reticulum, such as LC3II/I and p62. This phenomenon could be alleviated by adding cycloheximide (CHX), a protein synthesis inhibitor. We found that mTOR signaling pathway participated in paraptosis-like cell death induced by HNK in an autophagy-independent process. Moreover, the mitogen-activated protein kinase (MAPK) signaling pathway induced paraptosis of NB4 cells by promoting endoplasmic reticulum stress. In summary, these findings indicate that paraptosis may be a new way to treat APL, and provide novel insights into the potential mechanism of paraptosis-like cell death.

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