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

ABSTRACT: 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).

ORGANISM(S): Mus musculus

PROVIDER: GSE198438 | GEO | 2022/12/15

REPOSITORIES: GEO

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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.

2022-12-15 | GSE168037 | GEO

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 [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.

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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NRF2-dependent ECM - Nrf2-Mediated Fibroblast Reprogramming Drives Cellular Senescence by Targeting the Matrisome

Project description:Nrf2-mediated fibroblast reprogramming drives cellular senescence by targeting the matrisome. ECM was isolated from WT and NRF2-/- mouse fibroblasts and analyzed by label-free quantification.

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Transcriptome analysis reveals malignant and hypoxic signature of glioblastoma

Project description:Purpose:Glioblastoma (GBM) is the most common primary brain tumor in adults with poor prognosis and short medial survival after therapy. we have utilized U87-MG cell line as a human GBM cell model and human brain HEB cell line as non-neoplastic brain cell cultured in normoxia and 1% O2 hypoxia for transcriptional profiling to gain further insight into the molecular underpinnings that maintained the properties of GBM andclarify the molecular mechanism of hypoxia resistance of GBM. Methods:We have utilized U87-MG cell line as a human GBM cell model and human brain HEB cell line as non-neoplastic brain cell cultured in normoxia and 1% O2 hypoxia for transcriptional profiling. And validating the analysis results with specimens of GBM patients. Results: Firstly, the resulting data set revealed previously unknown proteins, including AKR1B1, MT2A, UBC, EEF1A1 and MTRNR2l2 in U87-MG cells, which promoted GBM characters through MAPK pathway. Meanwhile, we found that toll-like pathway was a new avenue mediating the function of inflammatory response in GBM. Furthermore, The results suggested that cytokine TGF-β1 and HIFs’ targeted genes, including HMOX1 and STC1 could be regard as hypoxic markers for GBM. Conclusion:Taken together, our study identified new potential biomarkers and illustrated the genes associated with inflammation in GBM. More importantly, the unique pattern to hypoxia implied new insight for the GBM research of hypoxia resistance and recurrence in future.

2019-09-11 | GSE77307 | GEO

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