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Phenotypic mapping of pathological crosstalk between glioblastoma and innate immune cells by synthetic genetic tracing

ABSTRACT: Phenotypic mapping of pathological crosstalk between glioblastoma and innate immune cells by synthetic genetic tracing

PROVIDER: PRJNA563577 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10079644_1.fastq.gz	Fastqsanger.gz
	SRR10079644_2.fastq.gz	Fastqsanger.gz
	SRR10079645_1.fastq.gz	Fastqsanger.gz
	SRR10079645_2.fastq.gz	Fastqsanger.gz
	SRR10079646_1.fastq.gz	Fastqsanger.gz

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Phenotypic mapping of pathological crosstalk between glioblastoma and innate immune cells by synthetic genetic tracing

Project description:Glioblastoma is a lethal brain tumor which exhibits heterogeneity and resistance to therapy. Our understanding of tumor homeostasis is limited by a lack of genetic tools to selectively identify tumor states and fate transitions. Here, we use glioblastoma subtype signatures to construct synthetic genetic tracing cassettes and investigate tumor heterogeneity at cellular and molecular level, in vitro and in vivo. Through synthetic locus control regions, we demonstrated that proneural glioblastoma is a hardwired identity, whereas the mesenchymal glioblastoma is an adaptive and metastable cell state driven by pro-inflammatory and differentiation cues and DNA damage, but not hypoxia. Importantly, we discovered that innate immune cells divert glioblastoma cells to a proneural-to-mesenchymal transition which confers therapeutic resistance. Our synthetic genetic tracing methodology is simple, scalable and widely applicable to study homeostasis in development and diseases. In glioblastoma, the method causally links distinct (micro)environmental, genetic and pharmacological perturbations and mesenchymal commitment.

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Project description:Glioblastoma is a lethal brain tumor that exhibits heterogeneity and resistance to therapy. Our understanding of tumor homeostasis is limited by a lack of genetic tools to selectively identify tumor states and fate transitions. Here, we use glioblastoma subtype signatures to construct synthetic genetic tracing cassettes and investigate tumor heterogeneity at cellular and molecular levels, in vitro and in vivo. Through synthetic locus control regions, we demonstrate that proneural glioblastoma is a hardwired identity, whereas mesenchymal glioblastoma is an adaptive and metastable cell state driven by proinflammatory and differentiation cues and DNA damage, but not hypoxia. Importantly, we discovered that innate immune cells divert glioblastoma cells to a proneural-to-mesenchymal transition that confers therapeutic resistance. Our synthetic genetic tracing methodology is simple, scalable, and widely applicable to study homeostasis in development and diseases. In glioblastoma, the method causally links distinct (micro)environmental, genetic, and pharmacologic perturbations and mesenchymal commitment. SIGNIFICANCE: Glioblastoma is heterogeneous and incurable. Here, we designed synthetic reporters to reflect the transcriptional output of tumor cell states and signaling pathways' activity. This method is generally applicable to study homeostasis in normal tissues and diseases. In glioblastoma, synthetic genetic tracing causally connects cellular and molecular heterogeneity to therapeutic responses.This article is highlighted in the In This Issue feature, p. 521.

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