Multimodal Single-Cell Analysis Reveals Two Distinct Radioresistant Stem-like and Progenitor Cell Populations in Murine Glioma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA596187 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10719821_1.fastq.gz | Fastqsanger.gz | |||
| SRR10719821_2.fastq.gz | Fastqsanger.gz | |||
| SRR10719822_1.fastq.gz | Fastqsanger.gz | |||
| SRR10719822_2.fastq.gz | Fastqsanger.gz | |||
| SRR10719823_1.fastq.gz | Fastqsanger.gz |
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Project description:Radiation therapy is part of the standard of care for gliomas and kills a subset of tumor cells, while also altering the tumor microenvironment. Previous work shows that tumor cells with stem-like properties preferentially survive radiation and give rise to glioma recurrence. Various techniques for enriching and quantifying cells with stem-like properties have been used, including the fluorescence activated cell sorting (FACS)-based side population (SP) assay, which is a functional assay that enriches for stem-like tumor cells. In these analyses, mouse models of glioma have been used to understand the biology of this disease and the therapeutic response, including the biology of the radiation response. We present here an analysis of combined SP and single-cell RNA sequencing of genetically-engineered mouse models of glioma to show a time course of cellular response to radiation. We identify and characterize two distinct tumor cell populations that are inherently radioresistant. In addition, we identify and characterize distinct effects of radiation on immune cell populations within the tumor microenvironment.
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Project description:We cumulatively radiated a glioblastoma cell line, U87MG, and screened radioresistant glioma cells. A transcriptome sequencing was performed to analyze the transcription differences between the raidoresistant and control cells.
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Project description:Radiation therapy is part of the standard of care for gliomas and kills a subset of tumor cells, while also altering the tumor microenvironment. Tumor cells with stem-like properties preferentially survive radiation and give rise to glioma recurrence. Various techniques for enriching and quantifying cells with stem-like properties have been used, including the fluorescence activated cell sorting (FACS)-based side population (SP) assay, which is a functional assay that enriches for stem-like tumor cells. In these analyses, mouse models of glioma have been used to understand the biology of this disease and therapeutic responses, including the radiation response. We present combined SP analysis and single-cell RNA sequencing of genetically-engineered mouse models of glioma to show a time course of cellular response to radiation. We identify and characterize two distinct tumor cell populations that are inherently radioresistant and also distinct effects of radiation on immune cell populations within the tumor microenvironment.
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Project description:We established radioresistant cell sublines, named as BxPC3/RR1 and BxPC3/RR2 which were derived from parental human pancreatic cancer cell line BxPC3. The miRNA expression profiles of the radioresistant pancreatic cancer cells were then compared with their parental cells. Three samples were analysed. miRNAs that were differentially expressed (increased or decreased in expression by M-bM-^IM-%1.5-fold) between the radioresistant and parental cells were identified.
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Project description:Background: Radiotherapy plays an important role in the multimodal treatment of breast cancer. The response of a breast tumour to radiation depends not only on its innate radiosensitivity but also on tumour repopulation by cells that have developed radioresistance. Development of effective cancer treatments will require further molecular dissection of the processes that contribute to resistance. Methods: Radioresistant cell lines were established by exposing MDA-MB-231, MCF-7 and ZR-751 parental cells to increasing weekly doses of radiation. The development of radioresistance was evaluated through proliferation and colony formation assays. Phenotypic characterisation included migration and invasion assays and immunohistochemistry. Intrinsic differences and changes in response to radiation between parental and radioresistant cells were investigated by whole-transcriptome gene expression analysis. Gene enrichment and pathway-focused analyses identified signalling networks differentially activated in radioresistant cells, which were confirmed by western blotting. Results: Proliferation and colony formation assays confirmed radioresistance. Radioresistant cells exhibited enhanced migration and invasion, with evidence of epithelial-to-mesenchymal-transition, and limited activation of DNA damage and apoptotic pathways in response to 2 Gy ionising radiation. Significantly, acquisition of radioresistance in MCF-7 and ZR-751 cell lines resulted in a loss of expression of both ERα and PgR and an increase in EGFR expression; based on gene analysis they changed subtype classification from their parental luminal A to HER2-overexpressing (MCF-7 RR) and normal-like (ZR-751 RR) subtypes, indicating the extent of phenotypic changes and cellular plasticity involved in this process. Whole-transcriptome gene expression analysis identified down-regulation of ER signalling genes and up-regulation of genes associated with PI3K, MAPK and WNT pathway activity in radioresistant cell lines derived from ER+ cells; this was confirmed by western blot, which showed increased p-AKT and p-ERK expression following radiation. Conclusions: This is the first study to date that extensively describes the development and characterisation of three novel radioresistant breast cancer cell lines through both genetic and phenotypic analysis. More changes were identified between parental cells and their radioresistant derivatives in the ER+ (MCF-7 and ZR-751) compared with the ER- cell line (MDA-MB-231) model; however, multiple and likely interrelated mechanisms were identified that may contribute to the development of acquired resistance to radiotherapy.
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Project description:Pediatric diffuse midline gliomas harboring the Histone 3 lysine 27-to-methionine mutation (H3K27M-pDMG) represent a highly heterogenous group of brain tumors characterized by intrinsic resistance to radiation therapy, the current standard of care. Recent evidence suggests that intratumor small extracellular vesicle (sEV)-mediated signaling plays an oncogenic role among glioma stem cell populations. However, the dynamics and functional roles of H3K27M-pDMG derived sEVs in the context of radiation-induced stress remain unclear. In this study, we characterize sEV uptake dynamics between H3K27M tumor cells, identify potential sEV surface proteins involved in the process, and demonstrate that radioresistant (RR) H3K27M-pDMG-derived sEVs confer radioprotective effects to radiosensitive (RS) H3K27M-pDMG cells at the population level. RR-sEVs induce metabolic and gene expression changes in RS cell populations within the timescale of EV uptake and internalization, leading to improved DNA repair following radiation-induced stress. Furthermore, we identified the proteins, microRNAs (miRNAs), and metabolites present in RR-sEVs, shedding light on the molecular cargo that may be responsible for these effects. Our findings provide insights into the intrinsic radioresistant properties mediated by H3K27M-pDMG-derived sEVs and propose novel targets for disrupting radioresistant intratumoral communication in H3K27M-pDMGs.
2025-06-02 | GSE286943 | GEO
Project description:Pediatric diffuse midline gliomas harboring the Histone 3 lysine 27-to-methionine mutation (H3K27M-pDMG) represent a highly heterogenous group of brain tumors characterized by intrinsic resistance to radiation therapy, the current standard of care. Recent evidence suggests that intratumor small extracellular vesicle (sEV)-mediated signaling plays an oncogenic role among glioma stem cell populations. However, the dynamics and functional roles of H3K27M-pDMG derived sEVs in the context of radiation-induced stress remain unclear. In this study, we characterize sEV uptake dynamics between H3K27M tumor cells, identify potential sEV surface proteins involved in the process, and demonstrate that radioresistant (RR) H3K27M-pDMG-derived sEVs confer radioprotective effects to radiosensitive (RS) H3K27M-pDMG cells at the population level. RR-sEVs induce metabolic and gene expression changes in RS cell populations within the timescale of EV uptake and internalization, leading to improved DNA repair following radiation-induced stress. Furthermore, we identified the proteins, microRNAs (miRNAs), and metabolites present in RR-sEVs, shedding light on the molecular cargo that may be responsible for these effects. Our findings provide insights into the intrinsic radioresistant properties mediated by H3K27M-pDMG-derived sEVs and propose novel targets for disrupting radioresistant intratumoral communication in H3K27M-pDMGs.
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Project description:This SuperSeries is composed of the following subset Series:; GSE9712: Detection of genes differentially expressed in radioresistant tumors; GSE9713: Detection of genes differentially expressed in radioresistant and radiosensitive tumors before and after irradiation; GSE9714: Interferon response of radioresistant and radiosensitive human head&neck tumor cell lines Experiment Overall Design: Refer to individual Series
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Project description:Pediatric diffuse midline gliomas harboring the Histone 3 lysine 27-to-methionine mutation (H3K27M-pDMG) represent a highly heterogenous group of brain tumors characterized by intrinsic resistance to radiation therapy, the current standard of care. Recent evidence suggests that intratumor small extracellular vesicle (sEV)-mediated signaling plays an oncogenic role among glioma stem cell populations. However, the dynamics and functional roles of H3K27M-pDMG derived sEVs in the context of radiation-induced stress remain unclear. In this study, we characterize sEV uptake dynamics between H3K27M tumor cells, identify potential sEV surface proteins involved in the process, and demonstrate that radioresistant (RR) H3K27M-pDMG-derived sEVs confer radioprotective effects to radiosensitive (RS) H3K27M-pDMG cells at the population level. RR-sEVs induce metabolic and gene expression changes in RS cell populations within the timescale of EV uptake and internalization, leading to improved DNA repair following radiation-induced stress. Furthermore, we identified the proteins, microRNAs (miRNAs), and metabolites present in RR-sEVs, shedding light on the molecular cargo that may be responsible for these effects. Our findings provide insights into the intrinsic radioresistant properties mediated by H3K27M-pDMG-derived sEVs and propose novel targets for disrupting radioresistant intratumoral communication in H3K27M-pDMGs.
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