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EMT-induced stemness and tumorigenicity are fueled by an oncogenic EGF/Ras pathway

ABSTRACT: Pre-EMT GIF14 cells treated with TGF-β1

ORGANISM(S): Mus musculus

PROVIDER: GSE44055 | GEO | 2014/02/19

SECONDARY ACCESSION(S): PRJNA188460

REPOSITORIES: GEO

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EMT-induced stemness and tumorigenicity are fueled by an oncogenic EGF/Ras pathway

Project description:Pre-EMT GIF14 cells treated with TGF-M-NM-21 Total RNA obtained from isolated GIF-14 cells from untreated and TGF-M-NM-21-treated sample

2014-02-19 | E-GEOD-44055 | biostudies-arrayexpress

EMT-induced stemness and tumorigenicity are fueled by the EGFR/Ras pathway.

Project description:Recent studies have revealed that differentiated epithelial cells would acquire stem cell-like and tumorigenic properties following an Epithelial-Mesenchymal Transition (EMT). However, the signaling pathways that participate in this novel mechanism of tumorigenesis have not been fully characterized. In Runx3 (-/-) p53 (-/-) murine gastric epithelial (GIF-14) cells, EMT-induced plasticity is reflected in the expression of the embryonal proto-oncogene Hmga2 and Lgr5, an exclusive gastrointestinal stem cell marker. Here, we report the concurrent activation of an EGFR/Ras gene expression signature during TGF-?1-induced EMT in GIF-14 cells. Amongst the altered genes was the induction of Egfr, which corresponded with a delayed sensitization to EGF treatment in GIF-14. Co-treatment with TGF-?1 and EGF or the expression of exogenous KRas led to increased Hmga2 or Lgr5 expression, sphere initiation and colony formation in soft agar assay. Interestingly, the gain in cellular plasticity/tumorigenicity was not accompanied by increased EMT. This uncoupling of EMT and the induction of plasticity reveals an involvement of distinct signaling cues, whereby the EGFR/Ras pathway specifically promotes stemness and tumorigenicity in EMT-altered GIF-14 cells. These data show that the EGFR/Ras pathway requisite for the sustenance of gastric stem cells in vivo and in vitro is involved in the genesis and promotion of EMT-induced tumor-initiating cells.

| S-EPMC3741305 | biostudies-literature

Vicious circle of LSD1 and TGF β1 promotes EMT of gastric cancer

Project description:Vicious circle of some key proteins is critical in the process of tumor development. Nevertheless, the mechanism of how the epigenetic modifiers are involved in was seldom reported and has not been clearly illustrated. We found the expression of lysine specific demethylase 1 (LSD1), the first identified histone lysine demethylase, is positively correlated with transforming growth factor beta 1 (TGF β1) in gastric cancer tissues and can be promoted by TGF β1 activated (p-EKR)-(NF-κB)-p300 signaling pathway, which resulted in the progression of epithelial-mesenchymal transition (EMT) in human gastric cancer cells. On the other hand, abrogation of LSD1 leads to the down regulation of TGF β1 as well as the EMT. But in benign cells, this circle was blocked by TGF β1 induced inactivation of ERK, which suggested the distinct roles of TGF β1 against LSD1 in gastric cancer cells and benign cells. This vicious cycle may illustrate a novel mechanism for EMT in gastric cancer mediate by TGF β1 and LSD1 but not in benign cells and may serve as a new strategy for the prevention of EMT for gastric cancer.

2016-07-19 | GSE84487 | GEO

Overexpression of PHF8 promotes an EMT-related gene signature in MCF10A cells

Project description:PHF8 exerts distinct functions in different types of cancer. However, the mechanisms underlying its specific functions in each case remain obscure. To establish whether overexpression of PHF8 regulates the TGF-β induced the epithelial-mesenchymal transition (EMT), we treated MCF10A-Mock (control) and MCF10A-PHF8wt (overexpressing wild-type PHF8) cells with TGF-β1 for 0, 24, 48 and 72 hours and performed RNA-seq in biological duplicates. Our data indicated that EMT gene signatures were significantly enriched in MCF10A-PHF8 cells with TGF-β1 treatment at all time points, strongly indicating that PHF8 overexpression induces a sustained EMT signaling program.

2016-10-26 | GSE74377 | GEO

The effects of TGF-β1-induced EMT on the transcriptional program in HaCaT cells

Project description:Investigation of the transcriptional profile of TGF-β1-induced EMT in HaCaT cells.

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Gene expression in an EMT model using an immortalized bronchial epithelial cell line induced by TGF-β1

Project description:This study aimed to establish an epithelial-mesenchymal transition (EMT) model with an immortalized human bronchial epithelial cell line, M-BE, and to identify an EMT signature gene set. The TGF-β1-induced M-BE cells got spindle-shaped fibroblast-like morphology and lost the cell-cell contact, with down-regulated expression of epithelial marker E-cadherin and up-regulated expression of mesenchymal markers N-cadherin and Vimentin. Examined by microarray, there were 2628 genes identified as significant EMT-related, including 1490 up-regulated genes (FC > 2, fdr < 0.01) and 1138 down-regulated genes (FC < 0.5, fdr < 0.01) in TGF-β1-induced M-BE cells.

2013-10-06 | GSE40374 | GEO

Expression data from EMT-derived NRK-52E cells before and after the AMPKα2 knockdown

Project description:Recent studies have shown that AMPKα2 can regulate epithelial-mesenchymal transition(EMT) processes during kidney fibrosis. However, the underlying mechanisms for AMPKα2 changes in renal tubular EMT remain unclear. TGF-β1 was used to induce epithelial-mesenchymal transition(EMT) in normal rat renal tubular epithelial (NRK-52E) cells. Gene microarray was used to analyze differential gene expression in EMT-derived NRK-52E cells before and after the AMPKα2 knockout

2019-12-18 | GSE141981 | GEO

LncRNA LETS1 promotes TGF--induced EMT and cancer progression

Project description:Transforming growth factor- (TGF-) signaling is a critical driver of epithelial–mesenchymal transition (EMT) and cancer progression. However, the regulatory roles of long non-coding RNAs (lncRNAs) in TGF--induced EMT and cancer progression are not well understood. Here, we identified an unannotated nuclear lncRNA LETS1 (LncRNA Enforcing TGF- Signaling 1) as a novel TGF-/SMAD target gene. Loss of LETS1 attenuates TGF--induced EMT, migration and extravasation in breast and lung cancer cells. LETS1 potentiates TGF-/SMAD signaling by stabilizing cell surface TGF- type I receptor (TRI) and thereby forms a positive feedback loop. Mechanistically, LETS1 inhibits TRI polyubiquitination by inducing the orphan nuclear receptor 4A1 (NR4A1) expression, a critical determinant of a destruction complex for inhibitory SMAD7. An unbiased interactome analysis identified the Nuclear Factor of Activated T Cells (NFAT5) as a protein partner of LETS1 to mediate activation of NR4A1 promoter. Overall, our findings characterize LETS1 as an EMT-promoting lncRNA and elucidate the mechanism by which nuclear LETS1 potentiates TGF- receptor signaling.

2023-07-31 | PXD037401 | Pride

Gene Transcriptional Variation of Hepatic Progenitor Cells after TGF- 1-Induced EMT Transition and EGF-Induced MET Reversion

Project description:TGF-b1 induces hepatic progenitor cells experience an epithelial-mesenchymal transition, and EGF could reverse this process via mesenchymal-epithelial transition. Yet, the mechanism underline these EMT and MET processes are not clear. The aim of this study is to reveal the genes with significant difference during these EMT and MET process in hepatic progenitor cells.

2021-04-23 | GSE165858 | GEO

Gene expression signitures in ARPE-19 cells treated with or without TGF-β1

Project description:To identify the dysregulated lncRNA and mRNA expression in ARPE-19 cells underwent EMT, we established a TGF-β1 induced EMT model of ARPE-19 cells. ARPE-19 cells were treated with or without 10 ng/ml TGF-β1 for 48 h. Total RNA are extracted and subjected to microarray assay (Arraystar Human LncRNA Microarray V3.0)

2021-08-11 | GSE105053 | GEO

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