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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE323014 | GEO | 2026/03/26

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 [scMulti-omics]

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microRNA profiles of meningiomas

Project description:Meningiomas, one of the most common human brain tumors, are derived from arachnoidal cells associated with brain meninges, usually benign and frequently associated with neurofibromatosis type 2. Here we define a human meningioma-typical miRNA profile and characterize effects of one down-regulated miRNA, miR-200a, on tumor growth. Elevated levels of miR-200a inhibited meningioma cell growth in culture and in a tumor model in vivo. Up-regulation of miR-200a decreased expression of transcription factors, ZEB1 and SIP1, with consequently increased expression of E-cadherin, an adhesion protein associated with cell differentiation. Down-regulation of miR-200a in meningiomas and arachnoidal cells resulted in increased expression of Î² -catenin and cyclin D1 involved in cell proliferation. miR-200a was found to directly target Î² -catenin mRNA, thereby inhibiting its translation and blocking Î² -catenin-Wnt signaling, frequently involved in cancer. A direct correlation was found between down-regulation of miR-200a and up-regulation of Î²-catenin in human meningioma samples. Thus, miR-200a appears to act as a multi-functional tumor suppressor miRNA in meningiomas through effects on the E-cadherin and Î² -catenin-Wnt signaling pathways. This reveals a previously unrecognized signaling cascade involved in meningioma tumor development and highlights a novel molecular interaction between miR-200a and Wnt signaling, thereby providing insights into novel therapies for meningiomas. 14 meningioma tumor samples were compared to 3 arachnoidal tissue control samples. Two technical replicates were performed for each sample. Normalization and processing included combining the data from technical replicates. The below table contains quantile-normalized data.

2010-06-24 | E-GEOD-17792 | biostudies-arrayexpress

microRNA profiles of meningiomas

Project description:Meningiomas, one of the most common human brain tumors, are derived from arachnoidal cells associated with brain meninges, usually benign and frequently associated with neurofibromatosis type 2. Here we define a human meningioma-typical miRNA profile and characterize effects of one down-regulated miRNA, miR-200a, on tumor growth. Elevated levels of miR-200a inhibited meningioma cell growth in culture and in a tumor model in vivo. Up-regulation of miR-200a decreased expression of transcription factors, ZEB1 and SIP1, with consequently increased expression of E-cadherin, an adhesion protein associated with cell differentiation. Down-regulation of miR-200a in meningiomas and arachnoidal cells resulted in increased expression of β -catenin and cyclin D1 involved in cell proliferation. miR-200a was found to directly target β -catenin mRNA, thereby inhibiting its translation and blocking β -catenin-Wnt signaling, frequently involved in cancer. A direct correlation was found between down-regulation of miR-200a and up-regulation of β-catenin in human meningioma samples. Thus, miR-200a appears to act as a multi-functional tumor suppressor miRNA in meningiomas through effects on the E-cadherin and β -catenin-Wnt signaling pathways. This reveals a previously unrecognized signaling cascade involved in meningioma tumor development and highlights a novel molecular interaction between miR-200a and Wnt signaling, thereby providing insights into novel therapies for meningiomas.

2009-08-25 | GSE17792 | GEO

DNA Methylation Signatures Differentiate Meningiomas from Normal Dura [OmniSNP]

Project description:Meningiomas are the most common primary brain tumor. Though typically benign with a low mutational burden, histopathologic analysis has poor predictive value for malignant behavior and there are no proven chemotherapies. Although DNA methylation patterns distinguish subgroups of meningiomas and have higher predictive value for tumor behavior than histologic classification, little is known about differences in DNA methylation between meningiomas and surrounding normal dura tissue. Using multimodal studies of meningioma/dura pairs, we identified 4 distinct DNA methylation patterns. Diffuse DNA hypomethylation of malignant meningiomas readily facilitated their identification from lower grade tumors by unsupervised clustering. All clusters and 12/12 meningioma-dura pairs exhibited hypomethylation of the gene promoters of a module associated with the craniofacial patterning transcription factor FOXC1 and its upstream lncRNA FOXCUT. Furthermore, we identified an epigenetic continuum of increasing hypermethylation of polycomb repressive complex target promoters with increased histopathologic grade suggesting progressive epigenetic dysregulation is associated with increasing tumor aggressiveness. These findings are a starting point for future investigations of the role of epigenetic dysregulation of FOXC1 and cranial patterning genes in early stages of meningioma formation as well as studies of the utility of polycomb inhibitors for treatment of aggressive meningiomas.

2023-06-22 | GSE176457 | GEO

DNA Methylation Signatures Differentiate Meningiomas from Normal Dura [HumanMethylation450]

2023-06-22 | GSE178139 | GEO

Genetic and epigenetic profiling identifies two distinct classes of spinal meningiomas

Project description:Spinal meningiomas account for 1.2-12% of all meningiomas and 25-45% of all spinal tumours. About 20% of intracranial, but also 4.6% of spinal meningiomas recur and require additional treatment. The classification of intracranial meningiomas has evolved considerably in recent years and uses genetic [1,2,4] as well as epigenetic parameters [3,5] in order to more precisely predict the patients’ prognosis and to lay the ground for therapeutic regiments that are adapted to the aggressiveness of a patient’s tumor. On the other hand, spinal meningiomas are missing in many of the large cohorts that were gathered for the molecular profiling of meningiomas. Also, they have never been thoroughly analyzed separately, and their classification still relies on histopathological findings solely. We analysed 65 tumour samples from 63 patients, who had histologically proven spinal meningioma to perform genetic and epigenetic profiling. Clinical features are described in Supplementary Table 1, online resource. T-distributed Stochastic Neighbor Embedding (t-SNE) analysis of genome-wide DNA methylation data shows that most spinal meningiomas separate from cranial meningiomas (Fig. 1A&B) and form two distinct clusters.

2022-10-12 | GSE212449 | GEO

Expression data from meningiomas and normal meninges

Project description:Correlate the gene expression profiles with the most relevant patterns of chromosome abnormalities (cytogenetic subgroups of meningiomas) and the gene expression profiles could help to explain the differences in clinical behaviour of meningiomas. The impact of tumor cytogenetics on the gene expression analyzed in meningiomas. Here, we analyzed the gene expression profiles (GEP) of 47 tumors and correlated them with the most clinical relevant cytogenetic subgroups of meningiomas, including diploid tumors, isolated -22/22q-, del(1p36) alone and complex karyotypes associated with del(1p36) and/or -14q. In addition, 4 samples containing purified RNA extracted from normal meningeal cells (BioChain Institute, Hayward, CA and US Biological, Swampscott, MA, USA) were also processed.

2013-01-05 | E-GEOD-43290 | biostudies-arrayexpress

GSTM1 null genotype underpins recurrence of NF2 meningiomas

Project description:Introduction: Meningiomas are the most common primary central nervous system (CNS) tumor in adults, comprising one-third of all primary adult CNS tumors. Although several recent publications have identified molecular alterations in meningioma including characteristic mutations, copy number alterations, and gene expression signatures, our understanding of the drivers of meningioma recurrence is limited. Objective: To identify gene expression signatures of 1p-22q-NF2- meningioma recurrence, with concurrent biallelic inactivation of NF2 and loss of chr1p that are heterogenous but enriched for recurrent meningiomas. Methods: Transcriptomic alterations present in recurrent versus primary 1p-22q-NF2- meningiomas were identified using RNA sequencing (RNA-seq) data in a clinically annotated cohort. Results: Recurrent 1p-22q-NF2- meningiomas were enriched for a newly identified GSTM1 null genotype compared to primary meningiomas that showed variable GSTM1 expression and independent external validation was performed. Conclusions: The GSTM1 null genotype is a novel biomarker of 1p-22q-NF2- meningioma recurrence that resolves heterogeneity in existing meningioma subtypes and may be used to guide future clinical management decisions on extent of treatment to improve patient outcomes.

2024-12-09 | GSE283616 | GEO

Transcriptomic profiling of meningiomas reveals SMARCB1 mutation-driven immunosuppression via IL-17/CSF1 axis

Project description:Meningiomas with SMARCB1 mutations exhibit distinct immunosuppressive microenvironments. This study performed RNA-seq profiling of 13 human meningioma samples and 1 control sample to identify molecular mechanisms underlying immune evasion. We discovered that SMARCB1 loss upregulates the IL-17/CSF1 axis, leading to increased tumor-associated macrophage infiltration and CD8+ T-cell exhaustion. These findings provide new targets for immunotherapy in refractory meningiomas.

2025-10-30 | GSE304666 | GEO

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