Project description:Drug treatments often result in dramatic changes in gene expression. Thus, we used microarray to uncover gene expression effects of fluvastatin treatment on ASPC1-GFP PDAC cells.
Project description:Cisplatin is a broad-spectrum anticancer drug, which is estimated to be administered to 40-80% of patients undergoing chemotherapy. However, its clinical utility is often limited due to factors that include acquired resistance of cancer cells to cisplatin. Because cisplatin is currently evaluated as a prospective agent for combined chemotherapy of pancreatic ductal adenocarcinoma (PDAC), we have investigated mechanisms involved in the acquired resistance of PDAC cells to cisplatin using gene expression study of two different parental-resistant pairs of PDAC cell lines. We have developed cisplatin-resistant cell lines AsPC1-R and BxPC3-R from their parental PDAC cell lines AsPC1 and BxPC3, respectively, by culturing them in medium with step-wise increasing concentration of cisplatin. Parental and resistant pairs of PDAC cells were analyzed by whole-transcript gene expression analysis.
Project description:Fluvastatin has been identified as novel inhibitors of metastasis in pancreatic cancer. In multiple in vivo and in vitro experiments the compounds phenotypic effects was validated. Since under drug treatment the transcriptomic changes in examined cell lines were rather small, we expected the underlying mechanistic effect to be on the level of the proteome and more importantly the phospho-proteome. To evaluate this assumption we performed label-free full proteome and phosphoproteomics experiments on Fluvastatin treated ASPC1 cells.
Project description:USP21 promotes PDAC tumor cells to bypass KRAS* dependency. To dissect the molecular mechanism, we conducted RNA-seq analysis comparing iKPC cancer cells overexpressing GFP, wildtype USP21 and enzyme-dead USP21 at day 3 after KRAS* extinction. KRAS*-expressing iKPC cells with GFP overexpression are positive control.
Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, which lacks effective therapies. We demonstrated that the transcription factor, HOXC6, was overexpressed in most PDACs, and its inhibition blocked PDAC tumor growth and metastasis. HOXC6 transcriptionally activated the tumor-promoting kinase MSK1. To identify the phosphorylation targets of MSK1 and the mediators of its function in AsPC1 cells, we utilized an unbiased TMT10-based phosphoproteomics analysis. To do so, we treated AsPC1 cells with MSK1 inhibitor SB-747651A and performed TMT10-based quantitative phosphoproteomics analysis and identified MSK1 phosphorylation targets.
Project description:The CREB binding protein inhibitor ICG-001 suppresses pancreatic cancer growth We used microarrays to detail global gene expression changes in the pancreatic cancer cell line AsPC1 following treatment with ICG-001 or siRNA-mediated knockdown of CTNNB1 (beta-catenin) AsPC1 cells were treated with 10uM ICG-001 or vehicle control (DMSO) for either 6 hours or 24 hours. AsPC-1 cells were also separately transfected with 20nM control siRNA or CTNNB1 siRNA for 48 hours. RNA was extracted at these time points for hybridization to Affymetrix microarrays
Project description:miRNAs are known to be involved in PDAC tumourigenesis. However, not many have been investigated in the context of TGFb-induced EMT. To identify novel miRNAs involved in this response, we performed a miRNA profiling study in PANC-1 cells treated with TGFb and additional PDAC lines with epithelial or mesenchymal characteristics.
Project description:Analysis of myofibroblast ablation at the gene expression level of PDAC tumors. Total RNA optained from pancreas of PDAC mice with and without aSMA myofibroblast ablated In addition, late stage aSMA ablated mice were treated with anti-CTLA4 treatment
Project description:The presence of some malignancies, such as cancer, impacts on peripheral blood mononuclear cells (PBMCs) gene expression profiling, suggesting the potential suitability of these genes as diagnostic and prognostic markers. The objective of this study was to identify new markers in peripheral blood that differentiate between PDAC patients and healthy controls as a means of facilitating early detection of the disease. 18 patients with unresectable PDAC were recruited. The diagnosis of PDAC was based on a positive biopsy of the pancreatic mass during the surgery. 18 gender, age, and habits matched healthy controls were also included. Whole genome cDNA microarray hybridization of PBMC samples was performed to identify potential PDAC markers.