ABSTRACT: The aim of the study was to characterize the role of GDF3 in NCCIT cells as a model of cancer stem cells. The NCCIT cells were stimulated for 3h with (1) 100ng/mL and (2) 300ng/mL GDF3, (3) 300ng/mL Nodal and (4) 100ng/mL GDF3 + 300ng/mL Nodal and compared to unstimulated control. Additionally a stable, lentiviral knockdown of GDF3 was performed in NCCIT cells and the transciption profile of these cells was compared to cells transduced with mock-virus. 5 conditions, 1 biological replicate each
Project description:The aim of the study was to characterize the role of GDF3 in NCCIT cells as a model of cancer stem cells. The NCCIT cells were stimulated for 3h with (1) 100ng/mL and (2) 300ng/mL GDF3, (3) 300ng/mL Nodal and (4) 100ng/mL GDF3 + 300ng/mL Nodal and compared to unstimulated control. Additionally a stable, lentiviral knockdown of GDF3 was performed in NCCIT cells and the transciption profile of these cells was compared to cells transduced with mock-virus.
Project description:This is an investigation of whole genome gene expression level in human coronary endothelial cells (HCAEC) and human pulmonary endothelial cells (HPAEC) stimulated by FK565 or LipidA. We show that parenteral administration of a pure synthetic Nod1 ligand, FK565, induces site-specific vascular inflammation in mice, which is prominent in and aortic root including aortic valves, slight in aorta and absent in other arteries. The in vitro production of proinflammatory chemokine/cytokine by FK565 is higher in HCAEC than in HPAEC, suggesting that site-specific vascular inflammation is at least in part ascribed to an intrinsic nature of the vascular cell itself. A six chip study using total RNA recovered from HCAEC and HPAEC which were stimulated by LipidA or FK565 in vitro. HCAEC and HPAEC were stimulated with FK565 (10µg/mL) or LipidA (100ng/mL) for 24 hours in 12-well plates (10,000 cells/cm2). Total RNA was extracted and subjected to RNA microarray analysis.
Project description:CXCL12 and IGF1 are key secreting molecules produced by cancer-associated fibroblasts in breast cancer. These factors promote the survival of disseminated cancer cells in the bone marrow. To assess the combined responses elicited by CXCL12 and IGF1, we examined the translating transcriptome of cancer cells in response to these two factors by Translating Ribosome Affinity Purification (TRAP)-RNAseq. MDA-MB-231 cells were engineered to express an EGFP-tagged version of ribosomal protein L10a. This allows the retrieval of polysome-associated mRNA by anti-GFP pull down (TRAP) and profiling the translating transcriptome by RNAseq. EGFP-L10a+ cancer cells were serum starved (0.2% serum) for 24 hours, and then treated with CXCL12 (30ng/mL) + IGF1 (10ng/mL) or CXCL12 (300ng/mL) + IGF1 (100ng/mL) for 6hrs. Two biological replicates were profiled for each condition.
Project description:This study investigates the effects of the aryl hydrocarbon receptor (AhR) ligands TCDD and PCB126 on hepatic gene expression in female sprague dawley rats. Rats were treated with toxicological equivalent doses of TCDD (100ng/kg/day) (Toxic equivalence factor (TEF) = 1.0), PCB126 (30ng, 300ng or 1000ng/kg/day) (TEF = 0.1) or a vehicle control of corn oil:acetone (99:1) 5 days a week for 52 weeks.
Project description:We performed quantitative label-free quantitative mass spectrometry (LFQ-MS) on 16 cell lysates and 16 EV lysates derived from BV2 microglia. These included four groups of BV2 cells (n=4/group) that were treated (72 hours) with either LPS (100ng/mL) to polarize to a pro-inflammatory state, IL-10 (50ng/mL) to polarize to a protective state, TGFβ (50ng/mL) to polarize to a homeostatic state or untreated controls