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: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:MHCC97H cell, a human hepatocellular carcinoma (HCC) cell line, was stably overexpressed with empty vector, ACOT12, or ACOT12(RR312,313EE) mutant (ACOT12m). These cells were then used for gene expression profiles analysis.
Project description:The prognosis of hepatocellular carcinoma (HCC) is poor due to the high incidence of intrahepatic metastasis. The aim of this study is to investigate the mechanism of intrahepatic metastasis in HCC via extracellular vesicles (EVs).
Project description:To reveal the HNRNPAB-regulated lncRNAs, we performed microarray analyses to screen differential lncRNAs in HCC cells after stable overexpression or knockdown of HNRNPAB. MHCC97H and HCCLM3 (HCC cell lines with high-metastatic potentials), PLC/PRF/5 and HepG2 (HCC cell lines with low-metastatic potentials) were used in this study. HepG2-control, HepG2-hnRNPAB, PLC/PRF/5-control, PLC/PRF/5-hnRNPAB, MHCC97H-control, MHCC97H-sh-hnRNPAB, HCCLM3-control, HCCLM3-sh-hnRNPAB were perpared with hU6-MCS-CBh-gcGFP-IRES-puromycin-shRNA-HNRNPAB/mock lentiviral and Ubi-MCS-SV40-EGFP-IRES-puromycin-HNRNPAB/mock cDNA lentiviral,respectively, each performed in triplicate.
Project description:To investigate the function of EGR1 in HCC growth, we established EGR1 knock out MHCC97H cells by CRISPR/Cas9 system and EGR1-overexpressing PLC/PRF5 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of EGR1 knock out MHCC97H cells and parental MHCC97H cells, EGR1-overexpressing PLC/PRF5 cells and control PLC/PRF5 cells.
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:In this work, we generated a MHCC97H proteome datasets by In-gel digestion on Orbitrap Fusion Lumos. We systematically compared RNC-seq and Ribo-seq in the context of proteome identification, especially when identifying protein isoforms from AS. We also demonstrated that the single-molecule long read sequencing technique identified thousands of new splice variants and guided the MS identifications of new protein isoforms.
Project description:The proteomic profiling of nine commonly used HCC cell lines Hep3B, HepG2, HepG2.2.15, HUH7, PLC/PRF/5, MHCC97L,MHCC97H,HCCLM3 and HCCLM6