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Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [ATAC-seq]

ABSTRACT: Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [ATAC-seq]

PROVIDER: PRJNA787087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17167155_1.fastq.gz	Fastqsanger.gz
	SRR17167155_2.fastq.gz	Fastqsanger.gz
	SRR17167156_1.fastq.gz	Fastqsanger.gz
	SRR17167156_2.fastq.gz	Fastqsanger.gz
	SRR17167157_1.fastq.gz	Fastqsanger.gz

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Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression

Project description:Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression

| PRJNA787082 | ENA

Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [RNA-seq]

Project description:Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [RNA-seq]

| PRJNA787088 | ENA

Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [scRNA-Seq]

Project description:Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [scRNA-Seq]

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Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [scRNA-Seq]

Project description:Oncogenic RAS/MAPK signaling drives metastatic squamous cell carcinomas (SCCs). These cancers are typified by high mutational burden, often featuring activating mutations in phosphatidylinositol-3-kinase (PI3K). Here we show that early in skin HRASG12V-induced oncogenesis, transitions from benign to malignant states are also marked by PI3K, this time super-activated through a temporal cascade of non-genetic events. Coupling clonal skin SCC genetic models with bulk and single-cell transcriptomics, chromatin-landscaping, lentiviral reporters, and lineage-tracing, we trace its roots. We show that following HRASG12V activation, oncogenic stem cells rewire their gene expression program. Initially, they produce an array of angiogenic factors, triggering a striking influx of vasculature and TGFβ into the microenvironment. Sparked by TGFβ-signaling, the stem cells induce leptin receptor (LEPR), which through the angiogenic influx activates LEPR-signaling to launch downstream PI3K-AKT-mTOR signaling. Our findings show how dynamic temporal crosstalk with the microenvironment, orchestrated by the stem cells, can drive the path to malignancy.

2022-10-09 | GSE207975 | GEO

Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [ATAC-seq]

2022-10-09 | GSE190414 | GEO

Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression [RNA-seq]

2022-10-09 | GSE190411 | GEO

Oncogenic RAS triggers stem cell: microenvironment crosstalk to drive malignant progression

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

2022-10-09 | GSE190415 | GEO

Wild type N-ras displays anti-malignant properties, in part by downregulating decorin

Project description:Previously, we have demonstrated that wild type N-ras (wt N-ras) harbors an anti-malignant effect against mutated Ras and in tumors without Ras mutations. To investigate the molecular bases of this anti-malignant activity, we have studied the potency of this anti-malignant effect in a model system against SV40 T. We show that wild-type N-ras (wt N-ras) counteracts the effects of SV40T in NIH3T3 cells as seen by a decrease in proliferation, anchorage independence and changes in migration). We also show that wt N-ras also elicits the same anti-malignant effects in some human tumor cell lines (HT1080 and MDA-MB-231). Through mRNA and microRNA (miRNAs) expression profiling we have identified genes and miRNAs modulated by wt N-ras potentially responsible for the anti-malignant effect. wt N-ras appears to mediate its anti-malignant effect by downregulating some of the targets of the TGFb pathway and decorin, which are able to reverse the inhibition of migration induced by wt N-ras. Our experiments show that the molecules that mediate the anti-malignant effect appear to be different than those modulated by transforming N-ras. The components of the pathways modulated by wt N-ras mediating its anti-malignant effects are potential targets for therapeutic intervention in cancer. We report that the N-ras proto-oncogene has anti-malignant effects and that it does so by modulating different genes than its oncogenic counterpart, which indicates that it should be activating different pathways.

2011-04-19 | GSE28678 | GEO

Wild type N-ras displays anti-malignant properties, in part by downregulating decorin

2011-04-19 | E-GEOD-28678 | biostudies-arrayexpress

Activation of the innate immune system accelerates growth in cooperation with oncogenic Ras.

Project description:Innate immunity in Drosophila acts as an organismal surveillance system that measures external stimuli or cellular fitness and triggers context-specific responses to fight infections and maintain tissue homeostasis. However, uncontrolled activation of innate immune pathways can be detrimental to the system. In mammals, innate immune signaling is often overactivated in malignant cells and contributes to tumor progression. Drosophila tumor models have been instrumental in the discovery of interactions between pathways that promote tumorigenesis, but little is known about whether and how the Toll innate immune pathway interacts with oncogenes. Here we use a Drosophila epithelial in vivo model to investigate the interplay between Toll signaling and oncogenic Ras.

2024-10-29 | GSE266879 | GEO

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