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Targeting Innate Immune Signaling in Glioma-Initiating Cells Impairs Self-Renewal and Radiation-Induced Cellular Plasticity

ABSTRACT: Targeting Innate Immune Signaling in Glioma-Initiating Cells Impairs Self-Renewal and Radiation-Induced Cellular Plasticity

PROVIDER: PRJNA1204364 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31857802_1.fastq.gz	Fastqsanger.gz
	SRR31857802_2.fastq.gz	Fastqsanger.gz
	SRR31857803_1.fastq.gz	Fastqsanger.gz
	SRR31857803_2.fastq.gz	Fastqsanger.gz
	SRR31857804_1.fastq.gz	Fastqsanger.gz

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Targeting Innate Immune Signaling in Glioma-Initiating Cells Impairs Self-Renewal and Radiation-Induced Cellular Plasticity

Project description:Purpose: Organisms constantly face environmental stressors that threaten their cellular and genomic integrity. In their response, pathogen-associated molecular patterns (PAMPs) and/or damage-associated molecular patterns (DAMPs) are detected by pattern recognition receptors (PRRs) and trigger the innate immune response. In this study we tested the hypothesis that DAMPs contribute to radiation-induced cellular plasticity in Glioblastoma (GBM). GBM is known to be organized hierarchically with a small number of glioma-initiating cells (GICs) driving treatment resistance and recurrences. Materials and Methods: Using patient-derived GBM specimens, we employed sphere forming capacity assays and in vitro extreme limiting dilution assays to examine how innate immune receptor signaling impacts the maintenance and self-renewal of GICs. By leveraging an imaging system for putative GICs we determined de novo induction of GICs from non-stem glioma cells. Results: We find that GIC maintenance after irradiation is mediated by cGAS-independent STING signaling, possibly involving signaling through TLR4 and TLR9. Induction of radiation-induced plasticity involves TLR3 signaling, with potential roles for other receptors and processes modulated by MyD88. Conclusion: These findings suggest that targeting innate immune signaling could prevent radiation-induced cellular plasticity for potential therapeutic benefit.

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Progastrin is essential for the survival and self-renewal of tumor-initiating cells in colorectal cancer

Project description:Using established human CRC cell lines, we showed that progastrin expression were enriched under conditions that promote tumor-initiating cells (TIC) self-renewal.

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Erythropoietin promotes breast tumorigenesis through tumor initiating cell self-renewal

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Expression profiling of sox11-expressing glioma-initiating cell-like cells

Project description:To identify factors involved in tumorigenicity of glioma-initiating cells (GICs), we compared gene expression in GIC-like cells with and without sox11 expression. We established sox11-expressing mouse glioma-initiating cell (GIC)-like cell line (NSCL61s), NSCL61s-sox11, which lost tumorigenicity when transplanted in vivo. We think that genes, which are differently expressed between NSCL61s and NSCL61s-sox11, would be new targets for glioma therapy.

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Expression profiles of mouse glioma-initiating cells.

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Project description:In the past few years, mammary cancer initiating cells (CICs) have been identified in mouse and human as a subpopulation of tumor cells that selectively posses tumor initiation and self-renewal capacity and the ability to give rise to bulk populations of non-tumorigenic cancer cells progeny through differentiation. They could also be responsible for tumor progression, metastasis, resistance to therapy and recurrence. Thus, the understanding of the pathways regulating CIC self-renewal, differentiation and tumorigenicity represents an important task in the development of effective anticancer therapies. To detect the set of genes associated to CIC in our mouse breast cancer model we analysed three prototypic situations: TUBO cells grown in DMEM under adherent conditions (called TDA in GSE26517 and epithelial bulk in GSE21451), TUBO cells grown in mammosphere medium under adherent conditions (called TMA in GSE26517), TUBO cells grown in mammosphere medium under low-attachment conditions (called mammospheres p1 in GSE21451), i.e. the conditions used to support the formation of mammospheres. This analysis led to the identification of growth factors and immune system-related genes, including toll-like receptor 2 (TLR2). The inhibition of TLR2 signaling pathway strongly impaired mammosphere generation, demonstrating the involvement of TLR2 in CSC self-renewal.

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