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FOXF1 defines the core-regulatory circuitry in gastrointestinal stromal tumor (GIST)

ABSTRACT: FOXF1 defines the core-regulatory circuitry in gastrointestinal stromal tumor (GIST)

PROVIDER: PRJNA417469 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6265800_1.fastq.gz	Fastqsanger.gz
	SRR6265800_2.fastq.gz	Fastqsanger.gz
	SRR6265810.fastq.gz	Fastqsanger.gz
	SRR6265820.fastq.gz	Fastqsanger.gz
	SRR6265860.fastq.gz	Fastqsanger.gz

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FOXF1 defines the core-regulatory circuitry in gastrointestinal stromal tumor (GIST)

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

2018-02-01 | GSE106626 | GEO

FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor.

Project description:The cellular context that integrates upstream signaling and downstream nuclear response dictates the oncogenic behavior and shapes treatment responses in distinct cancer types. Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specification and GIST tumorigenesis. Further, FOXF1 colocalizes with ETV1 at enhancers and functions as a pioneer factor that regulates the ETV1-dependent GIST lineage-specific transcriptome through modulation of the local chromatin context, including chromatin accessibility, enhancer maintenance, and ETV1 binding. Functionally, FOXF1 is required for human GIST cell growth in vitro and murine GIST tumor growth and maintenance in vivo The simultaneous control of the upstream signaling and nuclear response sets up a unique regulatory paradigm and highlights the critical role of FOXF1 in enforcing the GIST cellular context for highly lineage-restricted clinical behavior and treatment response.Significance: We uncover that FOXF1 defines the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function. The unique and simultaneous control of signaling and transcriptional circuitry by FOXF1 sets up an enforced transcriptional addiction to FOXF1 in GIST, which can be exploited diagnostically and therapeutically. Cancer Discov; 8(2); 234-51. ©2017 AACR.See related commentary by Lee and Duensing, p. 146This article is highlighted in the In This Issue feature, p. 127.

| S-EPMC5809271 | biostudies-literature

mRNA profiles in gastrointestinal stromal tumor (GIST) cell lines and GIST-associated fibroblast

Project description:To identify mRNA profiles in GIST and CAFs, we performed RNA sequencing analysis (RNA-seq) using GIST cell lines, GIST-T1 and GIST882, and CAFs.

2020-01-14 | GSE143547 | GEO

miRNA expression profile in GIST (gastrointestinal stromal tumor)

Project description:To clarify aberrantly expressed miRNAs affecting the biology of GIST, miRNA array was performed in 19 cases of GIST.

2013-03-01 | GSE36087 | GEO

ETV1 and FOXF1 cistrome in wildtype GIST48, GIST-T1, MDA-PCa2b, and ETV1 or FOXF1 knocked-down GIST48 cells

Project description:ETV1 and FOXF1 cistrome in wildtype GIST48, GIST-T1, MDA-PCa2b, and ETV1 or FOXF1 knocked-down GIST48 cells

| PRJNA417539 | ENA

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

Project description:Activating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GISTs). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable. Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined. The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines in the presence or absence of added FGF2 in vitro, and delayed tumor regrowth in vivo. In addition, inhibition of mitogen-activated protein kinase (MAPK) signaling by imatinib was not sustained in GIST cells. An extracellular signal-regulated kinase (ERK) rebound occurred through activation of FGF signaling, and was repressed by FGFR1 inhibition. Downregultation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells. We used micorarrays to quantify the gene expression levels in GIST cell lines.

2015-01-08 | GSE64762 | GEO

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

2015-01-08 | E-GEOD-64762 | biostudies-arrayexpress

Genome wide analysis of mouse gastrointestinal stromal tumors (GIST) in a mouse model of spontaneous GIST.

Project description:Analysis of mouse GIST tumors at the gene expression level. The purpose of the study was to identify immunomodulatory genes in mouse GIST tumors after in vivo treatment with the specific tyrosine kinase inhibitor imatinib mesylate.

2011-12-31 | GSE30416 | GEO

Distinct gene-expression-defined classes of gastrointestinal stromal tumor (GIST).

Project description:GIST is considered to invariably arise through gain-of-function KIT or PDGFRA mutation of the interstitial cells of Cajal (ICC). However, the genetic basis of the malignant progression of GIST is poorly understood. We analysed the expression levels of 54,613 probe sets in 32 surgical samples of untreated GIST of the stomach and small intestine with GeneChip Human Genome U133 Plus 2.0 arrays. Keywords: gene expression array-based, count

2008-06-15 | GSE8167 | GEO

Mapping of ETV1 genomic binding sites in gastrointestinal stromal tumor (GIST).

Project description:ETV1 is highly expressed in GIST and their presumed precursors--the interstitial cells of Cajal. ETV1 is required for survival for both GIST and ICC and regulates GIST signature genes. Here, using Illumina-Solexa based next-generation sequencing of ETV1 chromatin immunoprecipates (ChIP-Seq), we define ETV1 binding sites in the GIST48 cell line.

2010-10-14 | GSE22441 | GEO

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