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.
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.
Project description:HNRNPC plays an important role in HCC metastasis, HNRNPC knockdown by specific shRNA (HNRNPC-shRNA) significantly inhibited the migration and invasion of MHCC97H cells, while HNRNPC overexpression exerted the opposite effect. To elucidate the mechanisms by which HNRNPC facilitated HCC metastasis, we performed microarray analysis to compare the transcription profiling between the MHCC97H-shcontrol and MHCC97H-shHNRNPC cells.
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.
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)
Project description:Goal for this study is to identified miRNA involved in metastasis development using PLC8024 and MHCC97H derived cell lines. PLC8024 derived cell lines, PLC-PT (Primary Tumor) and PLC-LM (Lung Metastasis), and MHCC97H derived cell lines, MHCC97H-PT and MHCC97H-LM were compared using the Ncode miRNA microarray platform. The experiment were repeat twice with dye-swap.
Project description:Gene expression in Madin Darby canine kidney cells grown for 7 days to confluence on Transwell filters and exposed to HGF +/- inhibitors of the MAPK pathway (MAPK is one of the pathways activated when HGF binds to the CMET receptor tyrosine kinase). We used microarrays to detail the program of gene expression in MDCK cells and identified genes specifically regulated by HGF via the MAPK pathway. Keywords: signaling pathway analysis
Project description:Gene expression in Madin Darby canine kidney cells grown for 7 days to confluence on Transwell filters and exposed to HGF +/- inhibitors of the MAPK pathway (MAPK is one of the pathways activated when HGF binds to the CMET receptor tyrosine kinase). We used microarrays to detail the program of gene expression in MDCK cells and identified genes specifically regulated by HGF via the MAPK pathway. Keywords: signaling pathway analysis MDCK cells were selected for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain expression of genes regulated by the MAPK pathway following HGF induction.
Project description:To investigate the molecular mechanisms by which UBXN1 promotes tumorigenesis, we performed RNA sequence analysis of the MHCC97H cell line with and without UBXN1.