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MiR-376c down-regulation accelerates EGF-dependent migration by targeting GRB2 in the HuCCT1 human intrahepatic cholangiocarcinoma cell line

ABSTRACT: The biological significance of the down-regulation of miR-376c in HuCCT1 cells is unknown. We revealed that miR-376c significantly reduced EGF-dependent cell migration through its target GRB2 in HuCCT1 cells. To elucidate key molecules in EGF-dependent HuCCT1 migration, in which GRB2 upregulation is caused by abnormal suppression of miR-376c, we compared expression profiles of mRNAs affected by pre-miR-376c and siRNA targeting GRB2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47186 | GEO | 2013/05/23

SECONDARY ACCESSION(S): PRJNA205046

REPOSITORIES: GEO

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MiR-376c down-regulation accelerates EGF-dependent migration by targeting GRB2 in the HuCCT1 human intrahepatic cholangiocarcinoma cell line

Project description:The biological significance of the down-regulation of miR-376c in HuCCT1 cells is unknown. We revealed that miR-376c significantly reduced EGF-dependent cell migration through its target GRB2 in HuCCT1 cells. To elucidate key molecules in EGF-dependent HuCCT1 migration, in which GRB2 upregulation is caused by abnormal suppression of miR-376c, we compared expression profiles of mRNAs affected by pre-miR-376c and siRNA targeting GRB2. We compared expression profiles of mRNAs affected by pre-miR-376c and siRNA targeting GRB2 in EGF-treated HuCCT1 cells.

2013-05-23 | E-GEOD-47186 | biostudies-arrayexpress

Homo sapiens

Project description:MiR-376c down-regulation accelerates EGF-dependent migration by targeting GRB2 in the HuCCT1 human intrahepatic cholangiocarcinoma cell line

| PRJNA205046 | ENA

MiR-376c down-regulation accelerates EGF-dependent migration by targeting GRB2 in the HuCCT1 human intrahepatic cholangiocarcinoma cell line.

Project description: Not available

| S-EPMC3724868 | biostudies-literature

Grb2 interactome data with and without EGF stimulation

Project description:Growth factor receptor-bound protein 2 or Grb2 is an adaptor protein involved in signal transduction. It is widely expressed and integral to several cellular functions, including cell proliferation. We designed this study to capture interacting partners of Grb2 in absence and presence of epidermal growth factor (EGF). HEK 293 cells, expressing tagged Grb2, were cultured with SILAC labels in presence and absence of EGF. Grb2 interactome was enriched by immunoprecipitation and subjected to mass spectrometry. This data will help in understanding the regulatory effect of EGF stimulation on Grb2 protein and its interactors.

2019-03-05 | PXD012957 | Pride

Effect of Crenigacestat treatment in xenograft model of HUCCT1 intrahepatic cholangiocarcinoma

Project description:Intrahepatic Cholangiocarcinoma (iCCA) is a difficult type of cancer to diagnose, extremely aggressive and resistant to therapeutic options with an increased incidence and mortality over time. The overexpression of Notch pathway is implicated in iCCA to create an ecosystem that drives the tumor aggressiveness. Specifically, Notch1 is overexpressed in iCCA tissue of patients, playing an important role on tumor growth. Our purpose was to investigate the effectiveness of Crenigacestat in in vivo experiments, using Hucct1 injected in CD1 mice to generate an iCCA xenograft mouse model. In the present study, in order to explore modulated factors and genes by treatment we performed a transcriptomic analysis validated by Western Blotting and qRT-PCR on iCCA tumor masses of xenograft mice. Our results indicate that the treatment significantly inhibited Notch1 and HES1 genes and proteins triggering a strong immune response. Nevertheless, moderate fibrosis was shown in this model which may have hindered response to therapy to promote tumor progression. We used microarray technology to understand the molecular mechanisms affected by Crenigacestat in HUCCT1 xenograft model of intraepatic cholangiocarcinoma.

2022-04-27 | GSE150024 | GEO

CASC15 overexpression in HuCCT1 cholangiocarcinoma cell line

Project description:The aim of the study was to characterize the transcriptional profile of cholangiocarcinoma cell line HuCCT1 after transfection with a plasmid encodind the long isoform of CASC15 (Gene ID: 401237 ; RNA sequence: NR_015410.1).

2018-03-01 | GSE102110 | GEO

RNA sequencing identifies gene expression profile changes associated with CREB3L1 gene silencing by transcriptional interference in HuCCT1 cells

Project description:The goals of this study are to examine changes in the expression profiles of genes in HuCCT1 cells following CREB3L1 gene silencing. In this study, three groups of Si-Ctrl HuCCT1 cells and three groups of Si-CREB3L1 HuCCT1 cells were used to study the change in expression of the different genes after CREB3L1 gene silencing by RNA-seq.

2022-02-20 | GSE194088 | GEO

Effect of Crenigacestat treatment in xenograft model of HUCCT1 intrahepatic cholangiocarcinoma

Project description:Effect of Crenigacestat treatment in xenograft model of HUCCT1 intrahepatic cholangiocarcinoma

| PRJNA630916 | ENA

EGF Induces Migration Independent of EMT or Invasion in A549 Lung Adenocarcinoma Cells

Project description:Tumors and tumor surrounding tissues produce multiple growth factors that influence tumor cell behavior via different signal transduction pathways. Growth factors like transforming growth factor beta (TGFβ) and epidermal growth factor (EGF) were shown to induce proliferation, migration and invasion in different cell models. Both factors are frequently overexpressed in cancer and will often act in combination. Although both factors are being used as rational targets in clinical oncology, similarities and differences of their contributions to cancer cell migration and invasion are not fully understood. Here we compared the impact of TGFβ, EGF and the combination of both factors on A549 cells. Both factors stimulated A549 migration to a similar extent but with a different kinetic and the combination had an additive effect. While EGF-induced migration depended on activation of the mitogen-activated protein kinase (MAPK) pathway, this pathway was dispensable for TGFβ-induced migration despite a strong activation by TGFβ. Proteome analysis revealed an overlap in expression patterns of migration-related proteins and associated gene ontology (GO) terms by TGFβ and EGF but only TGFβ induced the expression of epithelial to mesenchymal transition (EMT)-related proteins like matrix metalloproteinase 2 (MMP2). EGF in contrast, made no major contribution to EMT marker expression on either the protein or the transcript level. In line with these expression patterns, EGF was unable to increase invasion of A549 cells on its own and failed to enhance TGFβ-induced invasion. Overall, these data suggest that TGFβ and EGF may partly compensate each other for stimulation of cell migration but abrogation of TGFβ signaling may be more suitable for antagonizing invasion.

2021-04-08 | PXD023024 | Pride

Sensitivity of cholangiocarcinoma cells to gemcitabine is affected by microRNA expression

Project description:We examined the relationship between miRNA expression and the sensitivity of CCA cells to Gem. Two intrahepatic CCA cell lines, HuH28 and HuCCT1 were used. HuCCT1 cells were more sensitive to Gem than were HuH28 cells. The miRNA expression profiles of HuH28 and HuCCT1 were determined by microarray analysis. Eighteen miRNAs were differentially expressed whose ratios over ± 2log2 between HuH28 and HuCCT1. Among these 18 miRNAs, ectopic overexpression of each of three downregulated miRNAs in HuH28 (miR-29b, miR-205, miR-221) restored Gem sensitivity to HuH28. Suppression of one upregulated miRNA in HuH28, miR-125a-5p, inhibited HuH28 cell proliferation independently to Gem treatment.

2013-06-02 | GSE47396 | GEO

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