Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential gene expression analysis identified determinants of cell fate plasticity during radiation-induced regeneration in Drosophila

ABSTRACT: Differential gene expression analysis identified determinants of cell fate plasticity during radiation-induced regeneration in Drosophila

PROVIDER: PRJNA757764 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15612137.fastq.gz	Fastqsanger.gz
	SRR15612138.fastq.gz	Fastqsanger.gz
	SRR15612139.fastq.gz	Fastqsanger.gz
	SRR15612140.fastq.gz	Fastqsanger.gz
	SRR15612141.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Differential gene expression analysis identified determinants of cell fate plasticity during radiation-induced regeneration in Drosophila

Project description:We used here a combination of lineage tracing, FACS and genome-wide RNAseq to identify two key changes that accompany hinge-to-pouch fate change: (1) repression of hinge determinants and (2) upregulation of ribosome biogenesis.

2021-12-19 | GSE182782 | GEO

Differential gene expression analysis identified determinants of cell fate plasticity during radiation-induced regeneration in Drosophila.

Project description:Ionizing radiation (IR) is used to treat half of all cancer patients because of its ability to kill cells. IR, however, can induce stem cell-like properties in non-stem cancer cells, potentiating tumor regrowth and reduced therapeutic success. We identified previously a subpopulation of cells in Drosophila larval wing discs that exhibit IR-induced stem cell-like properties. These cells reside in the future wing hinge, are resistant to IR-induced apoptosis, and are capable of translocating, changing fate, and participating in regenerating the pouch that suffers more IR-induced apoptosis. We used here a combination of lineage tracing, FACS-sorting of cells that change fate, genome-wide RNAseq, and functional testing of 42 genes, to identify two key changes that are required cell-autonomously for IR-induced hinge-to-pouch fate change: (1) repression of hinge determinants Wg (Drosophila Wnt1) and conserved zinc-finger transcription factor Zfh2 and (2) upregulation of three ribosome biogenesis factors. Additional data indicate a role for Myc, a transcriptional activator of ribosome biogenesis genes, in the process. These results provide a molecular understanding of IR-induced cell fate plasticity that may be leveraged to improve radiation therapy.

| S-EPMC8769364 | biostudies-literature

Targeting Innate Immune Signaling in Glioma-Initiating Cells Impairs Self-Renewal and Radiation-Induced Cellular Plasticity

Project description:Purpose: Organisms constantly face environmental stressors that threaten their cellular and genomic integrity. In their response, pathogen-associated molecular patterns (PAMPs) and/or damage-associated molecular patterns (DAMPs) are detected by pattern recognition receptors (PRRs) and trigger the innate immune response. In this study we tested the hypothesis that DAMPs contribute to radiation-induced cellular plasticity in Glioblastoma (GBM). GBM is known to be organized hierarchically with a small number of glioma-initiating cells (GICs) driving treatment resistance and recurrences. Materials and Methods: Using patient-derived GBM specimens, we employed sphere forming capacity assays and in vitro extreme limiting dilution assays to examine how innate immune receptor signaling impacts the maintenance and self-renewal of GICs. By leveraging an imaging system for putative GICs we determined de novo induction of GICs from non-stem glioma cells. Results: We find that GIC maintenance after irradiation is mediated by cGAS-independent STING signaling, possibly involving signaling through TLR4 and TLR9. Induction of radiation-induced plasticity involves TLR3 signaling, with potential roles for other receptors and processes modulated by MyD88. Conclusion: These findings suggest that targeting innate immune signaling could prevent radiation-induced cellular plasticity for potential therapeutic benefit.

2025-04-17 | GSE285563 | GEO

Radiation-Induced Cellular Plasticity Primes Glioblastoma for Forskolin-Mediated Differentiation [Day21]

Project description:Radiation-Induced Cellular Plasticity Primes Glioblastoma for Forskolin-Mediated Differentiation [Day21]

| PRJNA1204339 | ENA

Functional determinants of sensitivity to CDK4/6 inhibition or cell-cycle plasticity

Project description:Functional determinants of sensitivity to CDK4/6 inhibition or cell-cycle plasticity

| PRJNA611980 | ENA

Functional determinants of sensitivity to CDK4/6 inhibition or cell-cycle plasticity

Project description:Intrinsic or acquired resistance to clinically approved CDK4/6 inhibitors have emerged as a major obstacle that hinders their utility beyond ER+ breast cancer. Palbociclib-sensitive ER+ breast cancer models and pancreatic ductal adenocarcinoma (PDAC) models were employed to identify functional determinants of response. In all models tested the activation of RB and inhibition of CDK2 activity emerged as determinants of sensitivity. While depleting CDK4 and 6 was sufficient to limit proliferation in specific resistance setting, RB loss renders cells completely CDK4/6 independent. The main down-stream target in this context is the activation status of CDK2 which is suppressed with CDK4/6 inhibition in an RB-dependent fashion. The P27KIP1 protein levels are associated with plasticity/rigidity of the cell cycle and correlates with sensitivity to CDK4/6 inhibiion. Exogenous overexpression and pharmacological induction of P27KIP1 by targeting the MEK/ERK pathway enhances the cytostatic effect of palbociclib. Similar to cell-culture data, in vivo experiments revealed that combination treatment of palbociclib and trametinib in mice bearing PDAC PDXs elicited a robust anti-proliferative effect with a corresponding increase in p27 expression. Mice bearing MCF7 xenografts displayed a durable response in the presence of palbociclib; however, over the course of treatment few cells begin to evade the negative cell-cycle regulation. Based on multispectral staining, the MCF7 tumor cells that underwent RB inactivation in the presence of palbociclib harbored low p27 expression. Finally, we demonstrate that the cell-cycle plasticity that enables tumor models to evade the palbociclib mediated RB activation could be potently targeted using a clinically applicable CDK2 inhibitor.

2020-06-30 | GSE146788 | GEO

Fate plasticity of interneuron specification

Project description:Fate plasticity of interneuron specification

| PRJNA1167741 | ENA

Hnrnpa21 regulates myogenic fate plasticity

Project description:Hnrnpa21 regulates myogenic fate plasticity

| PRJNA639464 | ENA

Radiation-Induced Cellular Plasticity Primes Glioblastoma for Forskolin-Mediated Differentiation [Day 5]

Project description:Radiation-Induced Cellular Plasticity Primes Glioblastoma for Forskolin-Mediated Differentiation [Day 5]

| PRJNA1204337 | ENA

Determinants of gastric cancer immune escape identified from non-coding immune-landscape quantitative trait loci

Project description:Determinants of gastric cancer immune escape identified from non-coding immune-landscape quantitative trait loci