Whole-body fluorescence imaging demonstrated selective homing of the CNWM-INKEC peptide to KIM-1-overexpressing A498 renal tumor compared to KIM1-low expressing HepG2 liver tumor in mice.
When stably transfected and expressed in 3T3-F442A preadipocytes and H35 hepatoma cells, the intact human GAPDH gene is induced 10-fold by insulin in 3T3-F442A adipocytes and 3-fold by insulin in H35 hepatoma lines, which is similar to the induction obtained with the endogenous gene.
When AdAFPlacZ was injected into the s.c. established hepatoma in vivo, expression of the beta-galactosidase gene was confined to AFP-producing HCC xenografts.
We used the CRISPR/Cas9 technique to delete in mice the syntenic region on chromosome 8 to create a Dnajb1-Prkaca fusion and monitored the mice for liver tumor development.
We used a regimen of adoptive cell transfer incorporating vaccination (ACTIV), with recombinant vaccinia virus expressing gp100, to treat a range of tumors including orthotopic breast tumors and large liver tumors.<b>Results:</b> ACTIV therapy induced durable complete remission of a variety of Her2<sup>+</sup> tumors, some in excess of 150 mm<sup>2</sup>, in immunocompetent mice expressing Her2 in normal tissues, including the breast and brain.
We then investigated the interaction between macrophages (cell line THP-1) and six different human cancer cell lines (four NSCLCs, one osteosarcoma, and one hepatoma) and its effect on IL-8 mRNA expression using a macrophage/cancer cell coculture system, IL-8 mRNA expression in lung cancer cells, and macrophages being measured separately after coculture in the presence or absence of six anti-inflammatory agents, i.e., pentoxifylline, aspirin, indomethacin, dexamethasone, celecoxib (a selective cyclooxygenase-2 inhibitor), and pyrrolidine dithiocarbamate, a specific nuclear factor kappaB (NF-kappaB) inhibitor.
We tested whether the uremic toxin indoxyl sulfate (IS), an endogenous ligand of the transcription factor aryl hydrocarbon receptor, could change the expression of the following liver transporters involved in drug clearance: <i>SLC10A1</i>, <i>SLC22A1</i>, <i>SLC22A7</i>, <i>SLC47A1</i>, <i>SLCO1B1</i>, <i>SLCO1B3</i>, <i>SLCO2B1</i>, <i>ABCB1</i>, <i>ABCB11</i>, <i>ABCC2</i>, <i>ABCC3</i>, <i>ABCC4</i>, <i>ABCC6</i>, and <i>ABCG2</i> We showed that IS increases the expression and activity of the efflux transporter P-glycoprotein (P-gp) encoded by <i>ABCB1</i> in human hepatoma cells (HepG2) without modifying the expression of the other transporters.
We tested whether the uremic toxin indoxyl sulfate (IS), an endogenous ligand of the transcription factor aryl hydrocarbon receptor, could change the expression of the following liver transporters involved in drug clearance: <i>SLC10A1</i>, <i>SLC22A1</i>, <i>SLC22A7</i>, <i>SLC47A1</i>, <i>SLCO1B1</i>, <i>SLCO1B3</i>, <i>SLCO2B1</i>, <i>ABCB1</i>, <i>ABCB11</i>, <i>ABCC2</i>, <i>ABCC3</i>, <i>ABCC4</i>, <i>ABCC6</i>, and <i>ABCG2</i> We showed that IS increases the expression and activity of the efflux transporter P-glycoprotein (P-gp) encoded by <i>ABCB1</i> in human hepatoma cells (HepG2) without modifying the expression of the other transporters.
We tested RNAi effects by transfecting human hepatoma and pancreatic cancer cell lines with AS and sense (S) RNA expression plasmids corresponding to the exogenous luciferase gene or the endogenous c-raf gene in the form of complexes with a cationic lipopolyamine or a tumour-targeting peptide vector we developed.
We suggested that the lack of p53 response may confer a growth advantage on preneoplastic hepatocytes and may be an important factor in hepatic tumor promotion by 2-acetylaminofluorene and other genotoxic compounds.
We sought to determine whether PPM1A expression is downregulated and whether PPM1A downregulation is correlated with CYP3A4 repression in the tumor liver tissue of HCC patients.
We sought to determine whether PPM1A expression is downregulated and whether PPM1A downregulation is correlated with CYP3A4 repression in the tumor liver tissue of HCC patients.
We silenced NM23-H1 expression in human hepatoma and colon carcinoma cells and methodologically investigated effects on cell-cell adhesion, migration, invasion, and signaling linked to cancer progression.
We showed that the C3 gene is the direct target for peroxisome proliferator-activated receptor α (PPARα) in human hepatoma HepG2 cells and mouse liver.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.
We show that SDF-1 G protein-coupled receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), and SDF-1 mRNA are expressed in human hepatoma Huh7 cells, which secrete and bind SDF-1.