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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [10X scRNA-seq]

ABSTRACT: Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [10X scRNA-seq]

PROVIDER: PRJNA705942 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13826407_1.fastq.gz	Fastqsanger.gz
	SRR13826407_2.fastq.gz	Fastqsanger.gz
	SRR13826408_1.fastq.gz	Fastqsanger.gz
	SRR13826408_2.fastq.gz	Fastqsanger.gz
	SRR13826409_1.fastq.gz	Fastqsanger.gz

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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma.

Project description:Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma.

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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [p16]

Project description:Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [p16]

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

Project description: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 [RNA-seq]

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

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

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

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Cellular senescence in malignant cells promotes tumorigenesis in mouse and patient glioblastoma [10X scRNA-seq]

Project description:The goal of this study is to identify the senescent cells expressing high level of p16Ink4a (p16Ink4a Hi) in GBMs, at an early timepoint. We introduced the p16-3MR transgene in the GBM mouse model to selectively delete p16Ink4a Hi senescent cells upon ganciclovir (GCV) injection. We compared two p16-3MR+GCV to two WT+GCV control GBMs that were harvested 7 days after the last GCV injection. p16Ink4a Hi senescent cells were a subset of malignant cells, mostly grouped in the astrocyte cluster and to a lesser extend in the NP-like cluster. We also found that p16Ink4a Hi senescent cells deletion modifies the cell state of malignant cells and modulates the tumor microenvironment. This study allowed us to define a GBM senescence signature.

2022-12-15 | GSE168038 | GEO

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

Project description:The goal of this transcriptomic analysis is to decipher whether NRF2 pathway plays a role in the induction of pro-tumoral senescence in glioblastoma (GBM).

2022-12-15 | GSE198438 | GEO

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.

2022-12-15 | GSE168039 | GEO

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.

2022-12-15 | GSE168037 | GEO

DNA methylation patterns separate senescence from malignant transformation potential in human cells [methylation]

Project description:Replicative senescent cells reportedly share similar DNA methylation changes with cancer cells, which are purported to facilitate tumorigenesis in cells bypassing senescence. However, we now report biologically critical and distinct patterns of DNA methylation evolution between replicative and oncogene-induced senescence and transformation in a classic human cell transformation model. While overall DNA methylation losses and gains occur in both replicative senescent and transformed cells, the patterns evolve more programmatically for the former and stochastically for the latter. Oncogene-induced senescence is an acute process involving minimal changes to DNA methylation. The stochastic DNA methylation alterations in transformation mainly involve a set of pro-survival promoter CpG-island methylation events targeting genes controlling development and differentiation processes, while the senescence-specific promoter changes occur in genes involved in positive regulation of cellular biosynthesis and macromolecular metabolism. The above set of pro-survival promoter CpG-island hypermethylation events, but not the senescence-specific events, are prone to occur in primary tumors and aging tissues. Importantly, cells manifest senescence-specific epigenomic patterns very early during commitment to senescence, and while these “near-senescent” cells can be immortalized, they are refractory to transformation by H-Ras oncoprotein (H-rasV12). The senescence-specific methylation is retained during immortalization and transformation attempts, suggesting it does not function to promote tumorigenesis. Thus, abnormalities in cancer-related methylation has their origins in aging and not replicative senescence, and senescence-associated methylation potentially prevents malignant transformation.

2018-01-31 | GSE91069 | GEO

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