Project description:CD14+ human immature myeloid cells were treated with TGF-beta for increased periods of time to study the effects of TGF-beta in regulating the myeloid cell lineage and functions.
Project description:Global expression profile of human osteoblast treated with recombinant TGF-beta compared to human osteoblast treated with growth media alone Dye-swap design with 6 biological replicates. Three arrays performed with TGF-beta treated samples on channel 1 and media-alone treated on channel 2; three arrays performed with TGF-beta treated samples on channel 2 and media-alone on channel 1.
Project description:Advanced ovarian cancer is the most lethal gynecologic malignancy in the United States. Ovarian cancer cells are known to have diminished response to TGF-beta, but it remains unclear whether TGF-beta can modulate ovarian cancer cell growth in an indirect manner through cancer-associated fibroblasts (CAFs). Using transcriptome profiling analyses on TGF-beta-treated ovarian fibroblasts, we identified a TGF-beta-responsive gene signature in ovarian fibroblasts. Identifying TGF-beta-regulated genes in the ovarian microenvironment helps in understanding the role of TGF-beta in ovarian cancer progression. The human telomerase-immortalized ovarian fibroblast line NOF151 was treated with 5ng/mL of either TGF-beta-1 or TGF-beta-2. Total RNA was isolated from control samples and TGF-beta-treated fibroblasts samples at 48 hours post-treatment, followed by cDNA synthesis, IVT and biotin labeling. Samples were then hybridized onto Affymetrix Human Genome U133 Plus 2.0 microarrays. For each treatment group, three independent samples were prepared for the microarray experiment.
Project description:Primary murine hepatocytes were transfected with siRNA targeting Caveolin-1 directly after attachment (o/n). Next day, cells were treated with TGF-beta for 48 h. Experiment was performed in triplicate using primary cells from 3 donor mice.
Project description:The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We quantified the association of TGF-beta-activated fibroblasts with disease progression. To this end, we used as surrogates the gene expression programme upregulated by addition of TGF-beta to normal colon mucosa-derived fibroblasts (CCD-Co-18) in culture. CCD-Co-18 were seeded at 60% confluence and treated with TGF-β1. Gene expression profiles were measured in duplicate using HG-U133 plus 2.0. We used RMA background correction, quantile normalization and RMA summarization (Gautier et al., 2004). A TGF-β response signature was obtained by selecting genes with limma P-value < 0.05 and at least two fold up-regulation in TGF-β treated fibroblasts.
Project description:In order to identify the genes that are regulated by TGF-beta in glioma, we serum starved two glioma cell lines, U373MG and U87MG, for 16h and we treated them with vehicle,100pM TGF-beta, 2uM inhibitor of the TGF-beta Receptor I(TbRI)(LY2109761), or both 100pM TGF-beta plus 2uM TbRI for 3h. Then, cell were collected and total RNA was extracted.
Project description:Advanced ovarian cancer is the most lethal gynecologic malignancy in the United States. Ovarian cancer cells are known to have diminished response to TGF-beta, but it remains unclear whether TGF-beta can modulate ovarian cancer cell growth in an indirect manner through cancer-associated fibroblasts (CAFs). Using transcriptome profiling analyses on TGF-beta-treated ovarian fibroblasts, we identified a TGF-beta-responsive gene signature in ovarian fibroblasts. Identifying TGF-beta-regulated genes in the ovarian microenvironment helps in understanding the role of TGF-beta in ovarian cancer progression.
Project description:The goal of the study was to identify the effects of TGF-beta on primary human macrophages maturated under different conditions. Experiment Overall Design: For the analysis of TGF-beta effects macrophages were differentiated in the presence of IL-4 or IL-4 in combination with dexamethasone. After 5 days differentiation mature macrophages were stimulated by TGF-beta for 24 hours. In the case of IL-4/dexamethasone stimulation an additional data point was taken. In this case macrophages were also stimulated by TGF-beta for 3 hours. For every group 5 independent donors were taken.