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ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59022 | GEO | 2014/10/07

SECONDARY ACCESSION(S): PRJNA254143

REPOSITORIES: GEO

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ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-07 | E-GEOD-59022 | biostudies-arrayexpress

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells.

Project description:The RAS/ERK pathway is commonly activated in carcinomas and promotes oncogenesis by altering transcriptional programs. However, the array of cis-regulatory elements and trans-acting factors that mediate these transcriptional changes is still unclear. Our genome-wide analysis determined that a sequence consisting of neighboring ETS and AP-1 transcription factor binding sites is enriched near cell migration genes activated by RAS/ERK signaling in epithelial cells. In vivo screening of candidate ETS proteins revealed that ETS1 is specifically required for migration of RAS/ERK activated cells. Furthermore, both migration and transcriptional activation through ETS/AP-1 required ERK phosphorylation of ETS1. Genome-wide mapping of multiple ETS proteins demonstrated that ETS1 binds specifically to enhancer ETS/AP-1 sequences. ETS1 occupancy, and its role in cell migration, was conserved in epithelial cells derived from multiple tissues, consistent with a chromatin organization common to epithelial cell lines. Genome-wide expression analysis showed that ETS1 was required for activation of RAS-regulated cell migration genes, but also identified a surprising role for ETS1 in the repression of genes such as DUSP4, DUSP6 and SPRY4 that provide negative feedback to the RAS/ERK pathway. Consistently, ETS1 was required for robust RAS/ERK pathway activation. Therefore, ETS1 has dual roles in mediating epithelial-specific RAS/ERK transcriptional functions.

| S-EPMC4231772 | biostudies-literature

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (RNA-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration. mRNA profiles of luciferase knockdown (WT), ETS1 knockdown, and U0126 treated DU145 cells were generated using deep sequencing, in triplicate, using Illumina HiSeq. Knockdowns were stable shRNA expression from a lentiviral construct selected with puromycin.

2014-10-07 | E-GEOD-59020 | biostudies-arrayexpress

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (ChIP-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration. ChIP-sequencing of various transcription factors

2014-10-07 | E-GEOD-59021 | biostudies-arrayexpress

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (ChIP-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration.

2014-10-07 | GSE59021 | GEO

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells (RNA-Seq)

Project description:ETS1 and RAS/ERK regulate a common gene expression program in establishing enviroment suitable for prostate cancer cell migration.

2014-10-07 | GSE59020 | GEO

ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells

Project description:ETS1 is a genome-wide effector of RAS/ERK signaling in epithelial cells

| PRJNA254143 | ENA

Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-08-22 | E-GEOD-64195 | biostudies-arrayexpress

Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape

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

2015-08-22 | GSE64195 | GEO

Norcantharidin Suppresses Colon Cancer Cell Epithelial-Mesenchymal Transition by Inhibiting the ?v?6-ERK-Ets1 Signaling Pathway.

Project description:Norcantharidin (NCTD) is an efficacious anti-cancer drug that has been used in China for many years, but its underlying mechanism of action is still not fully understood. In the present study, we found that NCTD could induce morphological changes in colon cancer cells, causing a transition from a spindle-shaped morphology to a typical round or oval shape, which was indicative of a mesenchymal-epithelial transition (MET) process. Next, we investigated the mechanism by which NCTD induced the MET process. Using a transwell assay, we found that NCTD could suppress the migratory and invasive ability of colon cancer cells in a dose-dependent manner. Moreover, NCTD suppressed the expression of integrin ?v?6, MMP-3, and MMP-9 as well as the polymerization of F-actin, further supporting its suppressive effect on migratory and invasive ability. Furthermore, the expression of ?v?6, N-cadherin, vimentin and phosphorylated ERK was decreased, while the expression of E-cadherin was up-regulated. We verified that phosphorylated Ets1 was down-regulated substantially after treatment with NCTD. Taken together, our data demonstrated that NCTD could inhibit the EMT process of colon cancer cells by inhibiting the ?v?6-ERK-Ets1 signaling pathway. This study revealed part of the mechanism through which NCTD could reverse the EMT process in colon cancer.

| S-EPMC4742802 | biostudies-other

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