Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer

ABSTRACT: Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer

PROVIDER: PRJNA849928 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19682600.fastq.gz	Fastqsanger.gz
	SRR19682601.fastq.gz	Fastqsanger.gz
	SRR19682602.fastq.gz	Fastqsanger.gz
	SRR19681905.fastq.gz	Fastqsanger.gz
	SRR19681906.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 48

Similar Datasets

Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [RNA-Seq]

Project description:Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [RNA-Seq]

| PRJNA849935 | ENA

Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [ChIP-Seq]

Project description:Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [ChIP-Seq]

| PRJNA849933 | ENA

Drosophila CNS mitochondrial dysfunction with Ras/MAPK inhibition microarray

Project description:Mitochondrial dysfunction causes biophysical, metabolic and signalling changes that alter homeostasis and reprogram cells. We used a Drosophila model in which TFAM is overexpressed in the nervous system with or without Ras/MAPK pathway inhibition, by knock-down of the ETS transcription factor pointed, to investigate the how mitochondrial dysfunction and Ras/MAPK signalling affect the transcriptome. We used microarray analysis to investigate gene expression in cases of mitochondrial dysfunction in the CNS with or without Ras/MAPK pathway inhibition by knock-down of pointed (Pnt) and anterior open (Aop).

2018-05-05 | GSE114054 | GEO

Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer

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

2022-07-06 | GSE206269 | GEO

Hyperactive RAS/MAPK introduces cancer-specific mitotic vulnerabilities

Project description:We performed tanscriptional profiling of ARPE19 and four isogenic transformed cells lines in which Ras or two downstream pathways, MAPK or PI3K/mTOR, were up-regulated. The purpose of this study is to understand how Ras signaling impacts kinetochore function.

2022-09-21 | GSE172512 | GEO

Loss of primary cilia drives switching from Hedgehog to Ras/MAPK pathway

Project description:Basal cell carcinomas (BCCs) rely on Hedgehog (HH) pathway growth signal amplification by the microtubule-based organelle, the primary cilium. Despite naïve tumors responsiveness to Smoothened inhibitors (Smoi), resistance in advanced tumors remains frequent. While the resistant BCCs usually maintain HH pathway activation, squamous cell carcinomas with Ras/MAPK pathway activation also arise, with the molecular basis of tumor type and pathway selection still obscure. Here we identify the primary cilium as a critical determinant controlling tumor pathway switching. Strikingly, Smoi-resistant BCCs possess an increased mutational load in ciliome genes, resulting in reduced primary cilia and HH pathway activation compared to naive or Gorlin patient BCCs. Gene set enrichment analysis of resistant BCCs with a low HH pathway signature reveals increased Ras/MAPK pathway activation. Tissue analysis confirms an inverse relationship between primary cilia presence and Ras/MAPK activation, and primary cilia removal in BCCs potentiates Ras/MAPK pathway activation. Moreover, activating Ras in HH-responsive cell lines confers resistance to both canonical (vismodegib) and non-canonical (aPKC and MRTF inhibitors) HH pathway inhibitors, while conferring sensitivity to MAPK inhibitors. Our results provide new insights into BCC treatment and identify the primary cilium as an important lineage gatekeeper, preventing HH to Ras/MAPK pathway switching.

2018-10-10 | GSE120954 | GEO

Oncogenic ETS proteins regulate a Ras/MAPK gene expression program in the absence of MAPK signaling

Project description:Approximately 50% of prostate cancers have chromosomal translocations resulting in the over-expression one of four ETS family transcription factors. However, it is not known why these four four family members are selected for oncogenic roles, while other ETS proteins are not. We found that the four oncogenic ETS family members have a specific role in prostate cell migration. Using chromatin immunoprecipitation coupled with next-generation sequencing, this specific biological function was matched to a specific set of genomic targets highlighted by the presence of an AP-1 binding site. ETS/AP-1 binding sites are prototypical Ras-responsive elements, but oncogenic ETS proteins could activate a Ras/MAPK transcriptional program in the absence of MAPK activation. These findings indicate that the specific function of ETS proteins over-expressed in prostate cancer is the activation of a Ras/MAPK gene expression program in the absence of signaling pathway mutations. 16 samples were analyzed, comprised of four replicates each of four different biological conditions. RNA from U0126 treated RWPE-1 empty vector cell RNA serves as a control for each experiment. Cell lines have retroviral expression constructs expressing either empty vector, Flag-ERG, or Flag-ETV1.

2011-10-18 | E-GEOD-29438 | biostudies-arrayexpress

Hyperactive RAS/MAPK introduces cancer-specific mitotic vulnerabilities

Project description:Hyperactive RAS/MAPK introduces cancer-specific mitotic vulnerabilities

| PRJNA723590 | ENA

Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [ChIP-Seq]

Project description:In this study, human pancreatic ductal adenocarcinoma cells lines (KP4, MiaPaca2) were treated with the MEK inhibitor, Trametinib or DMSO for 48hrs prior to RNA-seq profiling to evaluate significant gene expression changes associated with MEK inhibition. To assess the role of transcription factors MYC and TFE3 in regulation of gene expression changes associated with MEK inhibition, we performed chromatin immunoprecipitation using antibodies against c-MYC and TFE3 in KP4 cells following 48hrs of Trametinib or DMSO treatment.

2022-07-06 | GSE206268 | GEO

Coordinated transcriptional and catabolic programs support iron dependent adaptation to RAS-MAPK pathway inhibition in pancreatic cancer [RNA-Seq]

2022-07-06 | GSE206267 | GEO