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Stem cell-associated heterogeneity in Glioblastoma results from intrinsic tumor plasticity shaped by the microenvironment

ABSTRACT: Stem cell-associated heterogeneity in Glioblastoma results from intrinsic tumor plasticity shaped by the microenvironment

PROVIDER: PRJNA526715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8715441_1.fastq.gz	Fastqsanger.gz
	SRR8715441_2.fastq.gz	Fastqsanger.gz
	SRR8715442_1.fastq.gz	Fastqsanger.gz
	SRR8715442_2.fastq.gz	Fastqsanger.gz
	SRR8715443_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Stem cell-associated heterogeneity in Glioblastoma results from intrinsic tumor plasticity shaped by the microenvironment

Project description:Cancer stem cells (CSCs) have been proposed to underlie the hierarchical organization of Glioblastoma (GBM) causing resistance to treatment, however the identity of CSCs in solid tumors remains largely elusive. Here we find that GBM cells expressing cell membrane CSC-associated markers do not represent a clonal entity defined by distinct functional properties and/or transcriptomic profiles, but rather a plastic state that most cancer cells can adopt. We show that phenotypic heterogeneity arises from non-hierarchical, reversible state transitions that are instructed by the microenvironment. While all tested cancer cell subpopulations survive and adjust their phenotype in vivo, their speed of plasticity differs resulting in variable tumor growth rates. Thus CSC-associated phenotypic heterogeneity is a result of stochastic reversible plasticity and increased tumorigenic potential in vivo correlates with fast adapting cell states.

2019-03-26 | GSE128195 | GEO

Stem cell-associated heterogeneity in Glioblastoma results from intrinsic tumor plasticity shaped by the microenvironment.

Project description:The identity and unique capacity of cancer stem cells (CSC) to drive tumor growth and resistance have been challenged in brain tumors. Here we report that cells expressing CSC-associated cell membrane markers in Glioblastoma (GBM) do not represent a clonal entity defined by distinct functional properties and transcriptomic profiles, but rather a plastic state that most cancer cells can adopt. We show that phenotypic heterogeneity arises from non-hierarchical, reversible state transitions, instructed by the microenvironment and is predictable by mathematical modeling. Although functional stem cell properties were similar in vitro, accelerated reconstitution of heterogeneity provides a growth advantage in vivo, suggesting that tumorigenic potential is linked to intrinsic plasticity rather than CSC multipotency. The capacity of any given cancer cell to reconstitute tumor heterogeneity cautions against therapies targeting CSC-associated membrane epitopes. Instead inherent cancer cell plasticity emerges as a novel relevant target for treatment.

| S-EPMC6467886 | biostudies-literature

Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

Project description:The nervous system has a tremendous capacity for experience-dependent plasticity. In response to changes in activity induced by environmental cues, many types of neurons undergo a process known as homeostatic plasticity, which serves to maintain overall network function in the face of mounting experience-dependent changes in synaptic strengths. Homeostatic plasticity involves both changes in synaptic scaling and regulation of intrinsic excitability. Increases in spontaneous firing and excitability of sensory neurons are evident in some forms of chronic pain in both animal models and in human patients. However, it is not known whether homeostatic plasticity is engaged in sensory neurons under normal conditions or whether dysfunction in these homeostatic mechanisms might contribute to the pathophysiology of chronic pain. To address these questions, we tested the impact of sustained depolarization on various measures of excitability in mouse and human sensory neurons. Depolarization induced by 30mM KCl induces a compensatory decrease in the excitability of both mouse and human sensory neurons. Moreover, we also find that voltage-gated sodium currents are robustly inhibited in mouse sensory neurons after chronic depolarization, thus contributing to the overall decrease in neuronal excitability and serving as a potential regulatory mechanism to drive intrinsic neuronal homeostatic control. Our results indicate that mouse and human sensory neurons undergo homeostatic regulation of intrinsic excitability in response to sustained depolarization. Decreased efficacy of these homeostatic mechanisms could potentially contribute to the development of pathological conditions, including chronic pain.

2024-01-31 | GSE236109 | GEO

Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

Project description:Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons

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Microglial colonization is shaped by intrinsic and extrinsic CSF-1 during early forebrain development

Project description:Microglial colonization is shaped by intrinsic and extrinsic CSF-1 during early forebrain development

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Synaptic and Intrinsic Plasticity Mediated by CCK-type Signaling Coordinates Behavioral Changes During Motivational State Shifts

Project description:Transitions from hunger to satiety involve multiple behavioral changes, including modulation and inhibition of feeding behavior. Cholecystokinin (CCK), a key satiety peptide in mammals, plays a critical role in these processes, though whether and how CCK might induce satiety via synaptic and intrinsic plasticity remain unclear. Here, we demonstrate that CCK acts as a classical brain-gut peptide in a protostome, mollusk Aplysia. CCK neurons, located in the gut, project centrally to release CCK at the site of the feeding pattern generator. In vivo, CCK reduced food intake, while in vitro, it shifted motor patterns towards egestion and inhibited feeding programs. Mechanistically, CCK primarily modulated the excitability of the egestive-promoting B20 interneuron and suppressed synaptic inputs to protraction motoneurons, thereby altering program type and inhibiting feeding program generation. These findings highlight the importance of both synaptic and intrinsic plasticity in specific circuit elements for implementing motivational shifts induced by satiety peptides.

2025-05-17 | GSE296741 | GEO

i-shaped antibody engineering enables conformational tuning of biotherapeutic receptor agonists

Project description:The ability to leverage antibodies to agonize disease relevant biological pathways has the potential to unlock new drug targets for clinical investigation. While antibodies have been successful as antagonists, immune mediators, and targeting agents, they are not readily effective at recapitulating the biological activity of natural ligands. Among the important determinants of antibody agonist activity is the geometry of target receptor engagement. Herein, we describe a novel engineering approach inspired by a naturally occurring Fab-Fab homotypic interaction that constrains IgG in a unique i-shaped conformation. i-shaped antibody (iAb) engineering enables potent intrinsic agonism of five tumor necrosis factor receptor superfamily (TNFRSF) targets. When applied to bispecific antibodies against the heterodimeric IL-2 receptor pair, constrained bispecific IgG formats recapitulate IL-2 agonist activity. Thus, iAb engineering represents a new tool to tune agonist antibody function and this work provides a framework for the development of intrinsic antibody agonists with the potential for generalization across broad receptor classes.

2023-12-18 | GSE246602 | GEO

ZNF180 modulates tumor intrinsic immunotherapy resistance in melanoma through driving plasticity [ATAC-seq]

Project description:ZNF180 modulates tumor intrinsic immunotherapy resistance in melanoma through driving plasticity [ATAC-seq]

| PRJNA1327257 | ENA

ZNF180 modulates tumor intrinsic immunotherapy resistance in melanoma through driving plasticity [RNA-Seq]

Project description:ZNF180 modulates tumor intrinsic immunotherapy resistance in melanoma through driving plasticity [RNA-Seq]

| PRJNA1327258 | ENA

Evidence for rRNA 2'-O-methylation plasticity: control of intrinsic translational capabilities of human ribosomes

Project description:Ribosomal RNAs (rRNAs) are main effectors of mRNA decoding, peptide-bond formation and ribosome dynamics during translation. Ribose 2'-O-methylation (2'-O-Me) is the most abundant rRNA chemical modification, and display a complex pattern in rRNA. 2'-O-Me was shown to be essential for accurate and efficient protein synthesis in eukaryotic cells. However, whether rRNA 2'-O-Me is an adjustable feature of the human ribosome and a means of regulating ribosome function remains to be determined. Here we challenged rRNA 2'-O-Me globally by inhibiting the rRNA methyl-transferase fibrillarin (FBL) in human cells. Using RiboMethSeq, a non-biased quantitative mapping of 2'-O-Me, we identified a repertoire of 2'-O-Me sites subjected to variation and demonstrate that functional domains of ribosomes are targets of 2'-O-Me plasticity. Using the cricket paralysis virus (CrPV) IRES element, as a model, coupled to in vitro translation, we show that the intrinsic capability of ribosomes to translate mRNAs is modulated through 2'-O-Me pattern and not by non-ribosomal actors of the translational machinery. Our results establish rRNA 2'-O-methylation plasticity as a mechanism providing functional specificity to human ribosomes.

2018-01-19 | GSE105248 | GEO

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