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Expression data from heat-damaged MHCC97H treated by HGF

ABSTRACT: Expression data from heat-damaged MHCC97H treated by HGF

PROVIDER: PRJNA445723 | ENA |

REPOSITORIES: ENA

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Expression data from heat-damaged MHCC97H treated by HGF

Project description:Incomplete heat-damaged MHCC97H ususlly recurred. The mechanism of how residual HCC cells survive sublethal heat stress and develop rapid outgrowth remains poorly understood. We used microarrays to detail the gene expression and identified distinct classes of up-regulated and downregulated genes under the treatment of HGF at different dosages.

2018-03-27 | GSE112349 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of HGF treated (HGF+) and matched control (HGF-) HepG2 cells

Project description:We report the high-throughput profiling of HGF treated liver cancer cell (HepG2) for differentiated genes analysis. We generated HGF stimulated and paired control HepG2 cells for 4 days. We find that tumor suppressor genes that are overexpressed and some tumor associated genes were downregulated, therefore reflect cell state and HGF induced anti-tumor potential. This study provides a potential framework for the research of HGF induced critical genes in the application of liver cancer therapy.

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Next Generation Sequencing Facilitates Quantitative Analysis of HGF treated (HGF+) and matched control (HGF-) HepG2 cells

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HepG2 Cell: Control vs. HGF treated

Project description:Transcription profile of HepG2 cells treated with hepatocyte growth factor and control cells Two condition experiment, Hep G2 vs. Hep G2-HGF. Biological replicates: 1 control and 1 HGF-treated (no replication)

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Expression data of RPTEC cells treated with/without HGF, aMD5-PEG11 and aMD5-BMH

Project description:We synthesized HGF mimic Met-agonist, which is a kind of Met high-affinity dimeric peptide that can activate the Met through dimerization of Met, and induce cell growth, migration, and branching morphogenesis in a similar manner to HGF. Here we detected the gene expression profile induced by HGF and artificial Met-agonist (aMD5-PEG11 and aMD5-BMH). HGF and aMD5-PEG11 show similar induction of gene expression pattern, including multicellular organismal development, multicellular organismal process and anatomical structure development.

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Differential expression of miRNAs in HGF treated SWAN-71 versus untreated control by next generation sequencing

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Expression data of HGF/cMET pathway in prostate cancer DU145 cell line

Project description:DU145 prostate cancer cells were treated with 25 ng/ml hepatocyte growth factor (HGF) or vehicle for 2, 8, or 24 hours. HGF stimulates the cMET protein, a tyrosine kinase transmembrane protein. The aim of this study is to determine the role of the HGF/cMET pathway in immature cells of established prostate cancer. HGF stimulation of DU145 prostate cancer cell line led to cell migration in culture, formation of sprouts in Matrigel and inhibition of growth. These biological effects went together with induction of a stem-like phenotype as defined by up-regulation of CD49b, CD49f, CD44 and SOX9, and down-regulation of CD24 on gene-expression arrays and quantitative PCR. The shift towards a stem-like phenotype was reflected by protein modifications on FACS, Western blot, and enhanced rapid adhesion to collagen I. Small molecules SU11274 and PHA665752 were able to inhibit both morphologic and molecular HGF effects.

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Differential expression of miRNAs in HGF treated HTR-8/SVneo versus untreated control by next generation sequencing

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Expression data of HGF/cMET pathway in prostate cancer DU145 cell line

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Expression data from MDCK cells exposed to HGF +/- MAPK inhibitors

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2007-11-20 | GSE9435 | GEO

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