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Unknown,Transcriptomics,Genomics,Proteomics

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EGF decreases the abundance of microRNAs that restrain oncogenic transription factors

ABSTRACT: Epidermal growth factor (EGF) stimulates cells by launching gene expression programs that are frequently deregulated in cancer. MicroRNAs, which attenuate gene expression by binding complementary regions in messenger RNAs, are broadly implicated in cancer. Using genome-wide approaches, we showed that EGF stimulation initiates a coordinated transcriptional program of microRNAs and transcription factors. The earliest event involved a decrease in the abundance of a subset of 23 microRNAs. This step permitted rapid induction of oncogenic transcription factors, such as c-FOS, encoded by immediate early genes. In line with roles as suppressors of EGF receptor (EGFR) signaling, we report that the abundance of this early subset of microRNAs is decreased in breast and in brain tumors driven by the EGFR or the closely related HER2. These findings identify specific microRNAs as attenuators of growth factor signaling and oncogenesis 24 conditions: time course of 8 hours of HeLa and MCF10A cells after EGF or SERUM stimulation

ORGANISM(S): Homo sapiens

SUBMITTER: roi avraham

PROVIDER: E-GEOD-40626 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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EGF decreases the abundance of microRNAs that restrain oncogenic transription factors

Project description:Epidermal growth factor (EGF) stimulates cells by launching gene expression programs that are frequently deregulated in cancer. MicroRNAs, which attenuate gene expression by binding complementary regions in messenger RNAs, are broadly implicated in cancer. Using genome-wide approaches, we showed that EGF stimulation initiates a coordinated transcriptional program of microRNAs and transcription factors. The earliest event involved a decrease in the abundance of a subset of 23 microRNAs. This step permitted rapid induction of oncogenic transcription factors, such as c-FOS, encoded by immediate early genes. In line with roles as suppressors of EGF receptor (EGFR) signaling, we report that the abundance of this early subset of microRNAs is decreased in breast and in brain tumors driven by the EGFR or the closely related HER2. These findings identify specific microRNAs as attenuators of growth factor signaling and oncogenesis

2012-09-06 | GSE40626 | GEO

Flotillin-2 regulates EGFR activation, degradation, and cancer growth

Project description:Epidermal growth factor receptor (EGFR) signaling is frequently dysregulated in a variety of cancers. The ubiquitin ligase Cbl regulates degradation of activated EGFR through ubiquitination and acts as an adaptor to recruit proteins required for trafficking. We used Stable Isotope Labeling with Amino Acids in Cell Culture (SILAC) mass spectrometry (MS) to compare Cbl complexes in the absence and presence of EGF stimulation. We identified over a hundred novel Cbl interactors, and a secondary siRNA screen found that knockdown of Flotillin-2 (FLOT2) led to increased phosphorylation and degradation of EGFR upon EGF stimulation in HeLa cells. In H441 cells, FLOT2 knockdown increased EGF-stimulated EGFR phosphorylation, ubiquitination, and downstream signaling, reversible by the EGFR inhibitor erlotinib. CRISPR knockout of FLOT2 in HeLa cells confirmed EGFR downregulation, increased signaling, and increased dimerization and trafficking to the early endosome. FLOT2 interacts with both Cbl and EGFR. Downregulation of EGFR upon FLOT2 loss is Cbl-dependent, as co-knockdown of Cbl and Cbl-b restored EGFR levels. Stable overexpression of FLOT2 in HeLa cells decreased EGF-stimulated EGFR phosphorylation and ubiquitination. Overexpression of wild type (WT) FLOT2, but not the soluble G2A FLOT2 mutant, inhibited EGFR phosphorylation upon EGF stimulation in HEK293T cells. FLOT2 loss induces EGFR-dependent proliferation and anchorage-independent cell growth. Lastly, FLOT2 knockout increases tumor formation and tumor volume in nude mice and NSG mice, respectively. These data demonstrate that FLOT2 negatively regulates EGFR activation and dimerization, as well as its subsequent ubiquitination, endosomal trafficking, and degradation. FLOT2 negatively regulates proliferation in vitro and in vivo.

2023-03-11 | PXD031988 | Pride

Homo sapiens

Project description:6KR-EGFR expressing MCF7 following EGF or HRG stimulation

| PRJNA246684 | ENA

Transcription profiling of human HeLa cells stimulated with epidermal growth factor vs. unstimulated sampled at multiple time points to investigate the temporal regulation of the cellular EGFR cascade

Project description:HELA cells derived from human cervical tumor were subjected to EGF stimulation for 0,20,40,60,120,240 and 480 minutes. We used microarrays to understand the temporal regulation of the cellular EGFR cascade. Experiment Overall Design: HELA cells were grown in DMEM supplemented with 10% FCS and antibiotics. Cells were serum deprived for 24 hours. Following stimulation with 10 ng/ml EGF for 0,20,40,60,120,240 and 480 minutes.

2007-11-02 | E-GEOD-6783 | biostudies-arrayexpress

Transcription profiling of human MCF10A mammary gland epithelial cells stimulated with epidermal growth factor vs unstimulated and sampled at multiple time points to investidage the temporal regulation of the cellular EGFR cascade

Project description:MCF10A cells derived from spontaneously immortalized normal human mammary epithelia were subjected to EGF/SERUM stimulation for 0,20,40,60,120,240 and 480 minutes. We used microarrays to understand the temporal regulation of the cellular EGFR cascade. Experiment Overall Design: MCF10A cells were grown in DME:F12 medium supplemented with antibiotics, [10 mg/ml insulin, 0.1 mg/ml cholera toxin, 0.5 mg/ml hydrocortisone, heat-inactivated horse serum (5%); defined as 'serum' in the text] and 10ng/ml EGF. Cells were serum deprived for 24 hours. Following stimulation with EGF/SERUM for 0,20,40,60,120,240 and 480 minutes.

2007-11-01 | E-GEOD-6784 | biostudies-arrayexpress

Suppression of MicroRNA-9 by Mutant EGFR Signaling Induces FOXP1 to Enhance Glioblastoma Tumorigenicity

Project description:The EGF-receptor (EGFR) is amplified and mutated in glioblastoma (GBM) where its common mutation, (∆EGFR, also called EGFRvIII) has a variety of activities that promote growth and inhibit death, thereby conferring a strong tumor-enhancing effect. This range of activities suggested to us that ∆EGFR might exert its influence through pleiotropic effectors and we hypothesized that microRNAs (miRs) might serve such a function. To test this, we determined the miR profiles of GBM cells with activated wild type EGFR (wtEGFR) and mutant EGFR (∆EGFR) to cells with non-activated EGFR or kinase dead ∆EGFR. To identify miRs regulated by EGFR, RNA from 2 different glioma cell lines (U87 and U373) were hybridized to miR expression arrays and analyzed. Each cell type was engineered to express wild type EGFR (wtEGFR), dead kinase ∆EGFR (DK) or ∆EGFR at elevated levels similar to those observed in primary glioblastomas displaying EGFR overexpression. Parental cells expressing endogenous EGFR and wtEGFR cells stimulated with EGF for 1hr were also included in the analyses.

2013-12-20 | E-GEOD-53504 | biostudies-arrayexpress

Expression data from HELA cells subject to EGF stimulation

2007-03-01 | GSE6783 | GEO

Suppression of MicroRNA-9 by Mutant EGFR Signaling Induces FOXP1 to Enhance Glioblastoma Tumorigenicity

2013-12-20 | GSE53504 | GEO

Expression data from MCF10A cells subject to EGF stimulation

Project description:MCF10A cells derived from spontaneously immortalized normal human mammary epithel were subjected to EGF/SERUM stimulation for 0,20,40,60,120,240 and 480 minutes. We used microarrays to understand the temporal regulation of the cellular EGFR cascade. Keywords: time course

2007-03-01 | GSE6784 | GEO

microRNA expression signature of monocyte-derived dendritic cells (DCs) from peripheral blood mononuclear cells (PBMCs)

Project description:In order to detect the microRNA expression profile of in vitro generated dendritic cells , purified monocytes from PBMCs were used as dendritic cell (DCs) precursors and were cultured in medium with cocktail for differentiation and maturation to immature dendritic cells (iDCs) and mature dendritic cells (mDCs). microRNA samples were isolated from precursor, iDCs and mDCs and used for microarray-based microRNAs expression profiles. To generate enough amount of immature DC (iDCs) and mature DCs (mDCs), monocytes were differentiated with GM-CSF and rhIL-4 for 2 days and maturated in the presence of TNF-α, IL-1β, IL-6 and PGE2 for another 2 days. With the anticipation to insight developmental-stage-specific microRNAs with potential functions related to monocyte derived DCs, global microRNAs expression profiling was set using microarray technology.microRNA expression profiles were performed in triplicate independent experiments starting for 3 groups of precursor, iDC and mDC generated from different blood donors.

2013-01-28 | E-GEOD-15036 | biostudies-arrayexpress

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