A Depolarization-Activation Strategy Targeting Microglia: Cuproptosis-Mediated Immune Re-sensitization Nanoplatform in Glioma Therapy
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo Sapiens
SUBMITTER: 
Tao Xie
PROVIDER: PXD074848 | iProX | Sun Feb 22 00:00:00 GMT 2026
REPOSITORIES: iProX
Similar Datasets
Project description:Glioblastoma multiforme (GBM) is a highly malignant brain cancer, and microglial cells play a critical role in its progression. Activation of microglia can either promote or inhibit GBM growth depending on the stage of tumour development and on the microenvironment. As current treatments for GBM have limited efficacy, there is an urgent need to develop novel strategies based on nanoplatforms for drug delivery and efficient targeting. This study investigated the microglial response and the therapeutic efficacy of dual cell membrane-coated and doxorubicin-loaded hexagonal boron nitride nanoplatelets, tested on human microglia and GBM cells. The results showed promising therapeutic effects on glioma cells and an M2 microglia polarization, highlighted through proteomic analysis.
2024-01-26 | PXD043557 | Pride
Project description:Modern therapy approaches fail to prevent high grade glioma recurrence. So, alternative ways need to be developed. Changing glioma cells’ fate is an alternative way to prevent tumor growth. Two-step protocol based on an antiproliferative G-quadruplex and small molecules triggering neural differentiation showed to be effective on glioblastoma cell cultures. This approach was named a differential therapy. In this paper, we broaden the spectrum of cell cultures to gliomas of II, III and IV grades, showing the universality of suggested protocol on a variety of cancer cells. We checked the reasonability of consistent addition of factors to the glioma cells. Moreover, we demonstrated a significant inhibition of tumor growth after injection of GQIcombi into 101/8 tumor in glioma rat model. Thus, the proposed strategy of influencing on cancer cell growth is applicable to be further translated for therapy use.
2024-01-09 | GSE250617 | GEO
Project description:Several independent microglia preparations performed on different days were plated onto wells of 24-well plates, and either left untreated (control), treated with the C6 glioma-conditioned medium, or treated with LPS.<br>For each culture condition, a number of RNA samples were prepared, with each sample then separately labeled and hybridized. These RNA samples were prepared from non-overlapping sets of wells from at least two microglia preparations, so they constitute biological replicates.
2012-12-14 | E-MEXP-2466 | biostudies-arrayexpress
Project description:Neuronal activity promotes high-grade glioma (HGG) growth. An important mechanism mediating this neural regulation of brain cancer is activity-dependent cleavage and secretion of the synaptic molecule and glioma mitogen neuroligin-3 (Nlgn3), but the therapeutic potential of targeting Nlgn3 in glioma remains to be defined. We demonstrate a striking dependence of HGG growth on microenvironmental Nlgn3 and determine a targetable mechanism of secretion. Patient-derived orthotopic xenografts of pediatric glioblastoma, diffuse intrinsic pontine glioma and adult glioblastoma fail to grow in Nlgn3 knockout mice. Glioma exposure to Nlgn3 results in numerous signaling consequences, including early focal adhesion kinase activation upstream of PI3K-mTOR. Nlgn3 is cleaved from both neurons and oligodendrocyte precursor cells via the ADAM10 sheddase. Administration of ADAM10 inhibitors robustly blocks HGG xenograft growth. This work defines the therapeutic potential of and a promising strategy for targeting Nlgn3 secretion in the glioma microenvironment, which could prove transformative for treatment of HGG.
2017-08-11 | GSE99045 | GEO
Project description:The obejctive of this study is to establish the therapeutic role of 6-thio-dG for gliomas in vitro and in vivo and to elucidate the anti-tumor mechanisms of 6-thio-dG in glioma cells. And the ultimate goal of this proposal is to demonstrate the potential of 6-thio-dG as a novel strategy for primary and recurrent glioma.
2021-09-13 | GSE160619 | GEO
Project description:The tumor microenvironment of glioblastoma (GBM) is characterized by a high proportion of glioma-associated macrophages/microglia (GAMs). We performed spatial analysis (Visium) to profile GAMs in human GBM.
2025-04-11 | GSE273432 | GEO
Project description:The paper describes a model of glioma.
Created by COPASI 4.26 (Build 213)
This model is described in the article:
A mathematical model of pre-diagnostic glioma growth
Marc Sturrock, Wenrui Hao, Judith Schwartzbaum, Grzegorz A. Rempala
J Theor Biol. 2015 September 7; 380: 299–308
Abstract:
Due to their location, the malignant gliomas of the brain in humans are very difficult to treat in advanced stages. Blood-based biomarkers for glioma are needed for more accurate evaluation of treatment response as well as early diagnosis. However, biomarker research in primary brain tumors is challenging given their relative rarity and genetic diversity. It is further complicated by variations in the permeability of the blood brain barrier that affects the amount of marker released into the bloodstream. Inspired by recent temporal data indicating a possible decrease in serum glucose levels in patients with gliomas yet to be diagnosed, we present an ordinary differential equation model to capture early stage glioma growth. The model contains glioma-glucose-immune interactions and poses a potential mechanism by which this glucose drop can be explained. We present numerical simulations, parameter sensitivity analysis, linear stability analysis and a numerical experiment whereby we show how a dormant glioma can become malignant.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models .
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide.
Please refer to CC0 Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000801 | BioModels
Project description: Not available
| S-EPMC6522842 | biostudies-literature
Project description:We used MHC-I immunopeptidomics to study how MTX-241F, a selective EGFR/PI3K inhibitor, alters antigen presentation in diffuse midline glioma (H3K27M) and glioblastoma xenografts. MHC-I–bound peptides from vehicle- and drug-treated tumors were profiled by LC–MS/MS to identify tumor- and treatment-specific peptides, including candidate brain-enriched biomarkers and immunotherapy targets.
2026-02-10 | PXD070941 | Pride
Project description:Glioblastoma is the most common and most devastating adult primary brain tumor. Despite aggressive multimodal therapy, the median survival is approximately one year after diagnosis. In recent years bone marrow-derived human mesenchymal stem cells (BM-hMSCs) have shown promise as cell-based delivery vehicles for anti-glioma therapeutics. This is largely due to their innate ability to migrate towards gliomas. Several studies have successfully demonstrated their use as delivery vehicles for anti-glioma agents. However, it is now evident that BM-hMSCs demonstrate variable tropism towards gliomas based on a clinically relevant glioma stem cell (GSC) model of GBM. In this study, we compared the proteomic profile of cancer and stromal cell populations in GSC xenografts that attract BM-hMSCs (‘attractors’) with those to do not (‘non-attractors’) in order to identify cell-signaling pathways that may modulate BM-hMSCs homing followed by targeted transcriptomic analysis of human gene sets related to glioma biology. We identified lower protein expression of fatty acid metabolism and glucose-dependent metabolic pathways in attractors. While transcriptomic analysis suggested that N-linked glycosylation was increased. Conversely, glucose metabolic pathways, including oxidative phosphorylation, were increased in the stromal cells present in attractors. The results presented here provide the first evidence for glucose metabolism, reactive oxidative species and lipid-mediated tumor inflammatory response, and N-linked glycosylation in the homing of BM-hMSC to GSC xenografts. Reciprocal expression of these pathways in the stromal cell population may suggest microenvironment cross-talk. Our studies provide new insights on the signaling correlates underlying the differential homing capacity of BM-hMSCs to GSC xenografts.
2016-02-17 | PXD001778 | Pride