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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE111542 | GEO | 2018/11/30

REPOSITORIES: GEO

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

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

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The Influence of Met Receptor Level on HGF-Induced Glycolytic Reprogramming in Head and Neck Squamous Cell Carcinoma

Project description:Head and neck squamous cell carcinomas (HNSCC) are known to overexpress a variety of receptor tyrosine kinases, such as the HGF receptor Met. Like other malignancies, there is a mutual interaction between the tumor cells and surrounding tissues and cells. We hypothesized that activation of HGF/Met signaling in HNSCC might influence glucose metabolism and therefore substantially changes the tumor microenvironment. To determine the effect of HGF, we used three established HNSCC cell lines and flow cytometry, western blot and RNA sequencing. Dynamic changes in glucose metabolism were measured real-time by an Extracellular flux analyzer. As expected, the cell lines exhibited different levels of Met and responded differently to HGF stimulation. As confirmed by RNA sequencing, the level of Met expression is associated with the number of upregulated HGF-dependent genes. Overall, Met stimulation by HGF leads to increased glycolysis, presumably mediated by higher expression of three key enzymes of glycolysis. These effects appear to be stronger in Methigh expressing HNSCC cells. Collectively our data supports the hypothesized role of HGF/Met signaling in metabolic reprogramming of HNSCC.

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Functional Comparison of the HGF/Met and MSP/Ron Systems in a Pancreatic Cancer Model

Project description:Pancreatic cancer is an aggressive disease with a poor prognosis for which current standard chemotherapeutic treatment options offer little survival benefit. In recent years, receptor tyrosine kinases (RTK)s have garnered interest as therapeutic targets to augment or replace standard chemotherapeutic therapies because of their high expression levels in various cancers and their ability to promote cell growth, migration, and survival. Met and Ron, which are homologous RTKs activated by the ligands hepatocyte growth factor (HGF) and macrophage stimulating protein (MSP), respectively, are over-activated in many of the least treatable cancers. In pancreatic adenocarcinoma, Met expression is linked to poor patient survival and Ron expression is generally higher in tumor samples relative to normal tissue, although its prognostic significance in pancreatic cancer remains unclear. Despite the structural homology between Met and Ron, studies that have directly compared the functional outcomes of these systems in any context are limited. To address this, we sought to determine if the HGF/Met and MSP/Ron systems produce overlapping or divergent contributions towards a malignant phenotype by performing a characterization of MSP and HGF driven signaling, behavioral, and transcriptomic responses in pancreatic cancer cells in vitro. We found HGF and MSP both encouraged cell migration and activated the MAPK/Erk pathway both at the transcript and protein level. HGF uniquely increased proliferation in addition to regulating a wider variety of transcripts compared to MSP. Although HGF and MSP produced a differing breadth of responses, overlapping pro-cancer signaling, behavioral, and transcriptional effects suggest dual inhibition of the MSP/Ron and HGF/Met systems in pancreatic cancer may provide a more complete anti-cancer effect compared to individually targeting either system.

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Transcriptional response of ovarian cancer cell lines to HGF and CDDP

Project description:HGF sensitizes ovarian cancer cells to chemotherapeutics, e.g. cisplatin (CDDP), through a signaling cascade activated by its MET oncogene encoded receptor and transduced by the p38MAPK. This cascade results in the regulation of a common set of transcripts in three ovarian cancer cell lines, with different genetic profiles and susceptibility to drugs. In order to elucidate the mechanism of HGF dependent cell sensitization to drugs, the transcriptional response of the three ovarian cancer cell lines to HGF and CDDP were studied by microarray based transcription profiling

2013-12-31 | E-GEOD-24589 | biostudies-arrayexpress

Human breast cancer cell line temporal response to Hepatocyte growth factor / scatter factor (HGF/SF)

Project description:To study the gene expression kinetics following activation of Met, one normal human breast epithelium and six human breast cancer cell lines with variable Met expression and activity, were treated with HGF/SF for 0, 10, 30min and 24 hours and subjected to cDNA array analysis

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Project description:The hepatocyte growth factor (HGF)/c-Met signaling pathway is known to mediate vascularization. We have previously demonstrated that expression of a human HGF transgene in the small airways produced mice (HGF TG) that were more susceptible to the tobacco carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). We also have observed that HGF TG mice display significantly enhanced vascularization in the lungs that increases over time compared to wild-type (WT) littermates. To analyze which genes might contribute to increased vascularization from HGF overexpression in the airways, RNA and protein were isolated from whole lungs of individual HGF TG and WT adult mice. We profiled the mRNA expression of several hundred genes representative of six biological pathways involved in transformation, angiogenesis, and tumorigenesis using two commercial microarrays. Significant changes in expression over a 1.5-fold boundary were also observed in lung tumors derived from NNK-treated HGF TG mice.

2010-12-31 | GSE20468 | GEO

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Project description:Effect of MET exon 14 skipping on gene expression stimulated or not by its ligand Hepatocyte Growth Factor (HGF) in pulmonary epithelial 16HBE cell line which undergone genome-editing by CRISPR-Cas9 technology.

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Transcriptional response of ovarian cancer cell lines to HGF and CDDP

2013-12-31 | GSE24589 | 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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Jafarnejad2019 - Mechanistically detailed systems biology modeling of the HGF/Met pathway in hepatocellular carcinoma

Project description:Hepatocyte growth factor (HGF) signaling through its receptor Met has been implicated in hepatocellular carcinoma tumorigenesis and progression. Met interaction with integrins is shown to modulate the downstream signaling to Akt and ERK (extracellular-regulated kinase). In this study, we developed a mechanistically detailed systems biology model of HGF/Met signaling pathway that incorporated specific interactions with integrins to investigate the efficacy of integrin-binding peptide, AXT050, as monotherapy and in combination with other therapeutics targeting this pathway. Here we report that the modeled dynamics of the response to AXT050 revealed that receptor trafficking is sufficient to explain the effect of Met-integrin interactions on HGF signaling. Furthermore, the model predicted patient-specific synergy and antagonism of efficacy and potency for combination of AXT050 with sorafenib, cabozantinib, and rilotumumab. Overall, the model provides a valuable framework for studying the efficacy of drugs targeting receptor tyrosine kinase interaction with integrins, and identification of synergistic drug combinations for the patients. Model is encoded by Johannes and submitted to BioModels by Ahmad Zyoud.

2020-03-20 | MODEL2003200001 | BioModels

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