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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [mir-NRF2]

ABSTRACT: Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [mir-NRF2]

PROVIDER: PRJNA815308 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18301730_1.fastq.gz	Fastqsanger.gz
	SRR18301730_2.fastq.gz	Fastqsanger.gz
	SRR18301731_1.fastq.gz	Fastqsanger.gz
	SRR18301731_2.fastq.gz	Fastqsanger.gz
	SRR18301732_1.fastq.gz	Fastqsanger.gz

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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [mir-NRF2]

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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [bulk RNA-seq]

Project description:GBM mouse model: The goal of this study is to compare the transcriptomic landscape at the endpoint of GBMs upon senescent cells deletion. We introduced the p16-3MR transgene in the GBM mouse model to selectively delete senescent cells expressing high level of p16Ink4a (p16Ink4a Hi) upon ganciclovir (GCV) injection. We compared p16-3MR+GCV GBMs to two control conditions, either WT+GCV or p16-3MR+GCV. We showed a slight decreased of p16Ink4a transcripts in p16-3MR+GCV compared to WT+GCV GBMs and GSEA demonstrated significant down-regulation of senescence pathways in p16-3MR+GCV GBMs compared to control GBMs. GBM-derived organoids: We used a mouse GBM-derived organoids model to further explore the function of Nrf2, that we identified as one potential trigger of the pro-tumoral action of p16Ink4a Hi malignant cells. We compared GBM-derived organoids treated with the senolytic ABT263 (Navitoclax; inhibitor of the anti-apoptotic proteins Blcl2 and BCL-xL) or vehicle (vhc) after 14 days in culture. We validated ABT263 efficacy via the significant downregulation of the expression of p16Ink4a, p15Ink4b and p21Cip1 senescent markers. We further identified upon senolytic treatment, downregulated genes encoding for SASP. Importantly, GSEA revealed a significant downregulation of Nrf2 pathway upon senolytic treatment.

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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [RNA-seq]

Project description:We performed a scRNAseq analysis conducted at the endpoint of our GBM mouse model. We compared differentially expressed up-regulated genes in p16Ink4a positive vs p16Ink4a negative malignant cells. The goal was to compare this dataset with two other transcriptomic datasets, to explore the upstream regulator(s) of senescence in malignant cells. We found that Nuclear Factor Erythroid 2 Like 2 (Nfe2l2) signaling pathway was enriched in the 3 data sets.

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Gene expression changes in fibroblasts with constitutively active Nrf2 reflect a senescence-associated secretory phenotype (SASP)

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