Project description:Purpouse: To compare the transriptome of CCD-18Co human colon fibroblasts treated with vehicle or Wnt3A. Methods: We treated triplicate plates of CCD-18Co cells with vehicle or Wnt3A during 24 h. Afterwards, we obtained total RNA and used it in RNA-seq experiments. Results: Our analysis rendered a total of 1136 differentially expressed genes (FDR<0.05), of which 662 were up-regulated and 474 were downregulated in response to Wnt3A. Conclusions: Wnt3A regulates a wide set of genes in CCD-18Co human colon fibroblasts
Project description:We obtained the gene expression signature from oxaliplatin-treated fibroblasts and quantified the association of oxaliplatin-activated fibroblasts with disease progression in colorectal cancer.
Project description:Differential methylation between human normal fibroblast cell CCD-18Co transfected with P16-Dnmt or pTRIPZ control vector was identified using Illumina HumanMethylation 850K array. The genome-wide methylation detection experiment was carried out by CapitalBio Technology Company.
Project description:We used microarrays to investigate gene expression changes in human colon normal fibroblasts exposed to a bitter orange extract enriched in flavanones (and previously subjected to in vitro gastro-duodenal digestion) to determine possible modulatory beneficial effects induced by these plant-derived compounds on the colon cells. Experiment Overall Design: We used ~90% confluent monolayers of colon CCD-18Co cells exposed to either small doses of pre-digested extract from bitter orange containing a mixture of flavanones (Treated) or equivalent quantities of digestive enzymes and salts (Control). Treatments were done in triplicate.
Project description:Pre-treatment metastatic (liver) biopsies were harvested prior to 5-FU and oxaliplatin therapy. CT imaging for response evaluation using WHO criteria was performed every 6 weeks.
Project description:Oxaliplatin is a widely used anti-cancer drug. It is part of treatment regimens for colorectal and pancreatic cancers, but it is tested in esophageal, biliary tract, gastric or hepatocellular cancers as well. Contrary to this wide application, there is only limited amount of information about oxaliplatin mechanism and response to treatment. We have performed whole-cell proteomic study to obtain cellular response induced by oxaliplatin. For this purpose we have treated CCRF-CEM cell line by 5xIC50 (29.3 μM) for half-time to caspase activation (240 min). The complex proteomic comparison was done on the treated vs. un-treated cells by high-resolution mass spectrometry. We have identified 4049 proteins in average from three biological replicates. From such pool just 76 proteins were significantly downregulated and 31 proteins upregulated in at least of two replicates. Both upregulated and dowregulated proteins are involved in DNA damage response, which is the most significant effect of platinum drugs. Downregulated proteins are split into three fractions. One fraction was centrosomal proteins or proteins involved in G2/M regulation. Second fraction was RNA processing proteins or proteins of processome of both ribosomal subunits. Downregulation of those proteins shows to ongoing nucleolar stress. Third fraction consisted of several ribosomal proteins. This should be sign of ribosomal stress. Nucleolar and ribosomal stress are stress responses manifesting by nucleolar shrinkage or and by inhibition of ribosomal biogenesis. Cellular response to oxaliplatin is thus DNA damage response, which triggers nucleolar and subsequent ribosomal stress.
Project description:To identify key drivers of oxaliplatin resistance, we collected and analyzed the DEGs between oxaliplatin-resistant and oxaliplatin-non-resistant patient samples
Project description:Canonical Hedgehog (Hh) signaling regulates the expression of genes that are critical to the patterning and development of a variety of organ systems. In adult, both ligand-dependent and ligand-independent Hh pathway activation are known to promote tumorigenesis. Recent studies have shown that in tumors promoted by Hh ligand, activation occurs within the stromal microenvironment (Yauch et al., 2009). In situ hybridization of the pathway target gene, Ptch1, shows that signaling is located at stromal perivascular fibroblast-like cells in xenograft tumor sections derived from Hh-expressing colorectal cancer cell lines. To study the downstream genes regulated by Hh signaling, we treated a primary human colon myofibroblast, CCD-18Co, with SHH (1 ug/ml) or no treatment (control) in serum-free medium supplemented with 0.1% BSA for 72 hrs and performed microarray analysis (Affymetrix U133P) on these samples. Three biological replicates of SHH stimulated and three replicates of unstimulated primary colon myofibroblast cells CCD-18Co were used in the experiment to analyze their gene expression.
Project description:Aim: mRNA profile of HCT116 human colon cancer cells to study the early response of cells to oxaliplatin exposure at low doses (0.5µM) Results: After treatment with oxaliplatin for 24h at 0.5µM, only a very small fraction of genes were mis-regulated. They fall mainly include P53-response genes, genes regulating inflammation, or genes regulating cytoskeleton.
