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Expression array analysis of the hepatocyte growth factor (HGF) invasive program

ABSTRACT: HGF stimulates mitogenesis, motogenesis and morphogenesis in most epithelial target cells. Selective inhibition of HGF signaling blocks spontaneous metastasis, but not primary tumor growth, in the prostate adenocarcinoma derived PC3M cell xenograft model. To identify the HGF activated genes and pathways that contribute to cell motility and invasion, i.e. the HGF invasive program, expression profiling was performed on PC3M cells that were untreated or were treated with human HGF (hHGF), which drives all 3 primary activities, or with human HGF/NK2 (hNK2) or murine HGF (mHGF), which drive motility and invasion but not proliferation in human cells. Differences in gene expression profiles among these four groups were used to distiniguish between events associated with invasion (resulting from hNK2 or mHGF treatment) from those associated with the combination of invasion and proliferation (resulting from hHGF treatment).

ORGANISM(S): Homo sapiens

PROVIDER: GSE71404 | GEO | 2015/08/25

SECONDARY ACCESSION(S): PRJNA291099

REPOSITORIES: GEO

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Expression array analysis of the hepatocyte growth factor (HGF) invasive program

Project description:HGF stimulates mitogenesis, motogenesis and morphogenesis in most epithelial target cells. Selective inhibition of HGF signaling blocks spontaneous metastasis, but not primary tumor growth, in the prostate adenocarcinoma derived PC3M cell xenograft model. To identify the HGF activated genes and pathways that contribute to cell motility and invasion, i.e. the HGF invasive program, expression profiling was performed on PC3M cells that were untreated or were treated with human HGF (hHGF), which drives all 3 primary activities, or with human HGF/NK2 (hNK2) or murine HGF (mHGF), which drive motility and invasion but not proliferation in human cells. Differences in gene expression profiles among these four groups were used to distiniguish between events associated with invasion (resulting from hNK2 or mHGF treatment) from those associated with the combination of invasion and proliferation (resulting from hHGF treatment). PC3M cells were left untreated or treated with hHGF, hNK2 or mHGF for 8, 16 or 32 hours prior to RNA extraction, cDNA preparation and array hybridization.

2015-08-25 | E-GEOD-71404 | biostudies-arrayexpress

c-Met activation leads to the establishment of a TGFb regulatory network required for bladder cancer invasion

Project description:Aberrant c-Met activation and upregulation of its cognate ligand HGF are frequently observed in bladder cancer and have been shown to regulate downstream pathways involved in proliferation, motility, and invasion. The precise mechanism underlying HGF/c-MET mediated invasion in bladder cancer is partly addressed by this microarray dataset. HGF activates the canonical TGFb signaling pathway to enhance epithelial mesenchymal transition and bladder carcinoma invasion.

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Transcriptomic and Proteomic Response of HC-04 to hepatocyte growth factor (HGF)

Project description:The routine study of human malaria liver-stage biology in vitro is hampered by low infection efficiency of human hepatocellular carcinoma (HCC) lines (<0.1%), poor understanding of steady-state HCC biology, and lack of appropriate tools for trace sample analysis. HC-04 is the only HCC that supports complete development of human malaria parasites. We hypothesized that HCCs are in various intermediate stages of the epithelial-mesenchymal transition (EMT) and HC-04s retain epithelial characteristics that permit infection. We developed an novel analytical approach to test this hypothesis viz. the HC-04 response to hepatocyte growth factor (HGF). We used online two-dimensional liquid chromatography tandem mass spectrometry (2D-LC-MS/MS) to quantify protein expression profiles in HC-04 pre-/post-HGF treatment and validated these results by RT-qPCR and microscopy. We successfully increased protein identification efficiency over offline-2D methods by 12-fold using less sample material, allowing robust protein quantification. We observed expected up-regulation and down-regulation of EMT protein markers in response to HGF, but also unexpected cellular responses. HC-04 is thus susceptible to HGF-mediated signaling but to a lesser degree than what we observed for HepG2, a widely used, but poor malaria HCC model. Our analytical approach to understanding the basic biology of HC-04 helps us understand the factors that may influence its utility as a model for malaria liver-stage development. We observed that HC-04 treatment with HGF prior to the addition of Plasmodium falciparum sporozoites did not facilitate cell invasion, arguing for unlinking the effect of HGF on malaria liver stage development from hepatocyte invasion. Finally, our 2D-LC-MS/MS approach and broadly applicable experimental strategy should prove useful in the analysis of various hepatocyte-pathogen interactions, tumor progression and early disease events.

2014-02-17 | PXD000682 | Pride

Transcriptomic and Proteomic Response of HC-04 to hepatocyte growth factor (HGF)

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

Project description:The goal of this study is to compare miRNAs expressed by HGF treated SWAN-71 cells to miRNAs expressed in untreated control SWAN-71 cells to identify micro RNAs which play a role during HGF-mediated SWAN-71 cell invasion

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

Project description:The goal of this study is to compare miRNAs expressed by HGF treated HTR-8/SVneo cells to miRNAs expressed in untreated control HTR-8/SVneo cells to identify micro RNAs which play a role during HGF-mediated HTR-8/SVneo cells invasion

2019-01-29 | GSE125767 | 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.

2021-12-30 | GSE133424 | GEO

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

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

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Project description:HGF-CM increases the proliferation and migration ability of DPSC (Dental pulp stem cells) in a dosage dependent manner, and facilitates the mineralization of DPSC by upregulating odotogenic genes. Although lack of in vitro evidence, DPSC and hGF-CM could be a promising combination for pulp regeneration in the future.

2022-10-29 | GSE201524 | GEO

Expression profiling in HGF (Hereditary Gingival Fibromatosis) patients

Project description:To identify dysregulated genes in HGF (Hereditary Gingival Fibromatosis) patients, expression profiling was performed using Affymetrix Human Genome U133 plus 2.0 arrays. Total RNA was extracted from gingival tissue specimens excised from two non-syndromic HGF patients, siblings in one family, and three normal controls. Quantity and integrity of the total RNA was measured and assessed by Nanodrop spectrophotometer (Thermo Fisher Scientific) and agarose gel electrophoresis. In brief, cDNA preparation, cRNA labeling, hybridization to Affymetrix Human Genome U133 plus 2.0 arrays, and chip scanning were performed in accordance with the manufacturer’s protocol (Affymetrix). *.CEL data from the raw chip scans were imported into the Partek GS 6.5 and normalized by RMA normalization algorithms. Comparisons between the HGF and control group were performed with one-way ANOVA (p≤0.05).

2019-12-31 | E-MTAB-7801 | biostudies-arrayexpress

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