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Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

ABSTRACT: Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

PROVIDER: PRJNA1022144 | ENA |

REPOSITORIES: ENA

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Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

Project description:GL261 cells are one of the most common mouse glioblastoma cells used for in vivo studies in a immunocompetent model. We analyze GL261 and stem cells derived from them (GL261-GSCs) using scRNA-Seq.

2024-03-28 | GSE244301 | GEO

Single-cell RNA-sequencing (scRNA-Seq) of GL261 and GL261-GSCs

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Single-nucleus RNA-sequencing (snRNA-Seq) of brain cells from tumor-bearing C57BL/6 mice

Project description:GL261-derived glioblastoma stem cells (GSCs) form aggressive tumors when implanted into the brains of C57BL/6 mice. We used snRNA-Seq to analyze GL261 and GL261-GSCs as well as tumor samples of 7 and 28 days of development.

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Longitudinal scRNA-Seq of immune cells from GL261 murine brain Tumors and MHC class II deficient tumor-mircoenvironments

Project description:Longitudinal phenotyping of T cells and myeloid cells in early (day 14) and late (day26) GL261 tumors. Single cell RNA sequencing of CD45+ immune cell from intracranial murine GL261-SIINFEKL tumors 20 days after inoculation. SIINFEKL-reactive T cells were sorted based on dextramer staining. Using time-resolved scRNA-seq of murine tumor-infiltrating immune cells from early (d14) and late stage (d26) syngeneic GL261 gliomas we observed constant MHCII expression by murine microglia over time and overall high but decreasing MHCII expression in late stage bbm indicating a dynamic process of MHCII expression. We show that loss of major histocompatibility complex (MHC) class II (MHCII)-restricted antigen presentation on bbm drives dysfunctional intratumoral tumor-reactive CD8+ T cell states through increased expression of Tox, a critical regulator of T cell exhaustion. By calculating the normalized abundance of T cell states along the pseudotime trajectory of SIINFEKL-reactive CD8+ T cells retrieved from myeloidMHCII-proficient and -deficient microenvironments, we found an enrichment of a distinct T cell state in myeloidMHCIIKO CD8+ T cells that was defined by peak expression of exhaustion markers. Mechanistically, MHCII-dependent activation of CD4+ T cells restricts myeloid-derived osteopontin that triggers a chronic activation of nuclear factor of activated T cells (Nfat)2 in tumor-reactive CD8+ T cells. In summary, we provide evidence that MHCII-restricted antigen presentation on bbm is a key mechanism to directly maintain functional cytotoxic T cell states in brain tumors.

2023-01-19 | E-MTAB-12523 | biostudies-arrayexpress

Single cell RNA-sequencing of GSCs and GBM tumours

Project description:Characterization of glioblastoma tumors and glioblastoma stem cell (GSCs) lines with single cell or single nuclei RNA-sequencing.

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RNA deep sequencing analysis of glioma stem cells(GSCs) and non-GSCs

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Project description:Single cell ATAC sequencing of SIINFEKL-reactive immune cell from intracranial murine GL261-SIINFEKL tumors 20 days after inoculation. SIINFEKL-reactive T cells were sorted based on dextramer staining. We show that loss of major histocompatibility complex (MHC) class II (MHCII)-restricted antigen presentation on bbm drives dysfunctional intratumoral tumor-reactive CD8+ T cell states through increased chromatin accessibility and expression of Tox, a critical regulator of T cell exhaustion.

2023-01-11 | E-MTAB-12512 | biostudies-arrayexpress

RNA-seq of co-culture experiment between human endothelial cells (HUVECs) and mouse glioma (Gl261) with or without Notch Inhibitor Gamma Secretase Inhibitor (GSI)

Project description:Increased awareness for the role for angiocrine factors in stem cell biology, in general, has suggested a role for angiocrine factors in the maintenance of GSC stemness and also there are reciprocal bi-directional signals from endothelial cells (ECs) to glioma (Gl261) and vice versa. To extend, refine and elucidate perfusion-independent modes of GBM-EC communication (i.e., distinguishing contact dependent or contact independent routes), we carried-out the following experiments: ECs from umbilical veins tagged with RFP (HUVEC-RFP) were cultured with mouse glioma line Gl261 fluorescently labelled with GFP (Gl261-GFP) until reaching confluency by 72 h post culturing. Cells were than harvested, RNA extracted, and the combined co-culture transcriptomes were sequenced from a generated cDNA library without prior separation of the respective cell types (sample named as Co). The Co transcriptome was compared to that of an artificial mixtures of the two cell types (Gl261-GFP and HUVEC-RFP) in the exact cells ratio attained by the end of the co-cluttering aided by FACS-based determination of the GFP/RFP ratio (sample named as Sep). In this procedure advantage was taken on the different species from which GBM and ECs are derived and specialized bioinformatics tools allowing to unambiguously assign the transcripts to their respective GBM (mouse) or EC (human) origins, thereby circumventing confounding factors associated with cell purification. Considering that contact-dependent EC signaling is primarily regulated by canonical Notch pathway and that the Notch pathway was reported to play a role in self-renewal of GSCs, we also treated GBM-EC co-cultures with the Notch pathway inhibitor Gamma secretase inhibitor (GSI) (or with the DMSO vehicle alone) for 24 h before harvesting.

2022-01-01 | E-MTAB-9604 | biostudies-arrayexpress

Transcriptome expression pattern of E11.5 PGCs, P2 GSCs, and CD49f+GSCs.

Project description:The cell identities of CD49f+GSCs were further identified by comparing them with the E11.5 PGCs and P2 GSCs. The transcriptomic analysis revealed that the CD49f+GSCs had 1/3 similar genes profile to the E11.5 PGCs and P2 GSCs. Further gene ontology (GO) analysis demonstrated that the E11.5 PGCs, P2 GSCs, and CD49f+GSCs shared the partial similar gene expression profile of pluripotency regulation signaling pathway, PI3K-AKT signaling, chemokine signaling, and HIF-1 signaling.

2017-11-09 | GSE106664 | GEO

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