Project description:we performed microarray-based gene expression profiling of HT-29, Ca9-22 and SLPI-deficient Ca9-22 cells for high-throughput analysis and for screening differentially expressed genes (DEGs)
Project description:We used the myoma model in conjunction with gene expression profiling with microarray data as an efficient tool for high throughput analysis and to screen for differentially expressed genes. Our aim was to identify candidates playing an important role in SLPI and/or MMP-promoted tumor invasion by comparing oral carcinoma Ca9-22 cells, which highly express secretory leukocyte protease inhibitor (SLPI) gene, with SLPI-deficient Ca9-22 cells. In oral carcinoma Ca9-22 and SLPI-deficient Ca9-22 (ÎSLPI) samples, gene expression profiling was performed with the Affymetrix Human Genome U133 Plus 2.0 Array. Two arrays for 2 cell lines were analyzed.
Project description:We used the myoma model in conjunction with gene expression profiling with microarray data as an efficient tool for high throughput analysis and to screen for differentially expressed genes. Our aim was to identify candidates playing an important role in SLPI and/or MMP-promoted tumor invasion by comparing oral carcinoma Ca9-22 cells, which highly express secretory leukocyte protease inhibitor (SLPI) gene, with SLPI-deficient Ca9-22 cells.
Project description:A gene expression profiles of human oral squamous cell carcinoma lines, HSC-2 and Ca9-22, cultured under hypoxic conditions (1% pO2 for 24 or 48 hours) were compaired with those under normoxic conditions (21% pO2).
Project description:A gene expression profiles of human oral squamous cell carcinoma lines, HSC-2 and Ca9-22, cultured under hypoxic conditions (1% pO2 for 24 or 48 hours) were compaired with those under normoxic conditions (21% pO2). Six arrays for 2 cell lines in 3 conditions were analyzed.
Project description:The goal is to identify an IL-22Fc specific gene signature in human intestinal epithelial cells in order to support PD biomarkers for IL-22Fc. We have identified IL-22Fc specific activity in HT-29 cells as secreted acute phase proteins only in the presence of IL-1β. Therefore, HT-29 cells (from gCell) will be cultured with IL-22, IL-1β, IL-6 (as a pSTAT3 activation control) as well as IL-22 + IL-1β and IL-6 + IL-1β. The "SAMID" sample characteristic is a sample identifier internal to Genentech. The ID of this project in Genentech's ExpressionPlot database is PRJ0027983 Keywords: Expression profiling by array
Project description:Metastasis and drug-resistance are major problems in cancer chemotherapy. The purpose of this work was to analyze the molecular mechanisms underlying the invasive potential of drug-resistant colon carcinoma cells. Cellular models included the parental HT-29 cell line and its drug-resistant derivatives selected after chronic treatment with either 5-fluorouracil (5-FU), methotrexate (MTX), doxorubicin (DOX) or oxaliplatin (OXA). Drug-resistant invasive cells were compared to non invasive cells using cDNA microarray, qRT-PCR, flow cytometry, immunoblots and ELISA. Functional and cellular signaling analyses were undertaken using pharmacological inhibitors, function-blocking antibodies, and silencing by retrovirus-mediated RNA interference. 5-FU- and MTX-resistant HT-29 cells expressing an invasive phenotype in collagen type I and a metastatic behaviour in immunodeficient mice exhibited high expression of the chemokine receptor CXCR4. Macrophage migration inhibitory factor (MIF) was identified as the critical autocrine CXCR4 ligand promoting invasion in drug-resistant colon carcinoma HT-29 cells. Silencing of CXCR4 and impairing the MIF-CXCR4 signaling pathways by ISO-1, pAb FL-115, AMD-3100, mAb 12G5, and BIM-46187 abolished this aggressive phenotype. Induction of CXCR4 is associated with up-regulation of two genes encoding transcription factors previously shown to control CXCR4 expression (HIF-2a and ASCL2) and maintenance of intestinal stem cells (ASCL2). Enhanced CXCR4 expression was detected in liver metastases resected from colon cancer patients treated by the standard FOLFOX regimen. Combination therapies targeting the CXCR4-MIF axis can potentially counteract the emergence of the invasive metastatic behaviour in clonal derivatives of drug-resistant colon cancer cells. Samples: HT-29 cell clones were obtained by limiting dilution from HT-29 subpopulations resistant to methothrexate (HT-29 5M21 cell clone) and or to 5-Fluoro-uracil (HT-29 5F7 and HT-29 5F31). Samples were provided by Dr. T Lesuffleur. Xenografts: HT-29 5M21, HT-29 5F7, and HT-29 5F31 xenografts were obtained by a first subcutaneous inoculation of cells in Nude mice and then fragments of subcutaneous tumors were reimplantated in SCID mice. First experiment of microarrays: HT-29 5M21 and HT-29 5F7 cells (that are invasive in in vitro assays on type I collagen) were compared to HT-29 5F31 cells (that are not invasive in vitro on type I collagen). Samples were co-hybridized on Agilent Human 44K GEP arrays (respectively 5F31 vs 5M21, 5F31 vs 5F7, 5M21 vs 5F31 and 5F7 vs 5F31). Second experiment of microarrays: HT-29 5M21 and HT-29 5F7 xenografts (that develop metastases in immuno-deficient mice lungs) were compared to HT-29 5F31 xenografts (that do not develop metastases in immuno-deficient mice lungs). Samples were consequently co-hybridized on human and mouse 4x44K GEP arrays (respectively AG41_5F31-5M21-138869, AG39_5F31-5F7-138867, AG42_5M21-5F31-138870 and AG40_5F7-5F31-138868 for human microarrays; 5M21_5F31_27033_4, 5F31_5M21_27033_3, 5F7_5F31_27033_2 and 5F31_5F7_27033_1_1 for mouse microarrays).
Project description:MIEN1 has been described as a key actor in colorectal cancer (CRC) biogenesis. We have used CRISPR/Cas9 technique to delete the promoter region of MIEN1 in HT-29 CRC cells. RNA-seq experiments revealed that several biological processes related to migration/metastasis were enriched by differentially expressed genes. Genetically modified cells shown decreased migration capacity.
Project description:Identify candidate different expression genes in HT-29 cells after incubation with Bifidobacterium bifidum ATCC 29521. The results of microarray provide importment information for different genes expression in HT-29 cell after incubation withBifidobacterium bifidum ATCC 29521, up or down-regulated.
