Project description:This study examines the transcriptional changes invoked by the novel anti-cancer agent PTC596 in AsPC-1 pancreatic cancer cells as compared to DMSO.
Project description:TGF-beta treatment of Panc-1 pancreatic adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments. The goal of the experiment is to profile temporal gene expression changes during TGF-beta-induced epithelial-mesenchymal transition (EMT). During EMT cancer cells lose their epithelial specifc proteins and gain mesenchymal proteins to acquire migratory and invasive phenotype essential for metastasis. Human Panc-1 pancreatic adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 48 h to induce EMT. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques.
Project description:TGF-beta treatment of Panc-1 pancreatic adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments. The goal of the experiment is to profile temporal gene expression changes during TGF-beta-induced epithelial-mesenchymal transition (EMT). During EMT cancer cells lose their epithelial specifc proteins and gain mesenchymal proteins to acquire migratory and invasive phenotype essential for metastasis. Human Panc-1 pancreatic adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 48 h to induce EMT. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques. Human Panc-1 pancreatic adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 48 h. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques.
Project description:Perineural invasion (PNI) is a unique biological feature of pancreatic cancer and is a key cause of pancreatic cancer metastasis, recurrence and poor postoperative survival, but its mechanism is largely unclarified. Clinical sample analysis and endoscopic ultrasonographic elasticity scoring indicated that cancer-associated fibroblasts (CAFs) are closely related to the occurrence of PNI. Furthermore, CAF-derived extracellular vesicles played an extremely important role in PNI in a dorsal root ganglion (DRG) coculture model and sciatic nerve model. To explore the lncRNA packaged in CAFs EVs transmitted to PANC-1, we conducted the lncRNA profile of PAN-1 treated with CAFs derived EVs.
Project description:To explore the whole transcriptional regulation of lncRNA and mRNA expression in hydrogen peroxide (H2O2) signaling, we used human pancreatic normal epithelial cell line hTERT-HPNE and pancreatic cancer cell line PANC-1 for H2O2 treatment and utilized transcriptome sequence to analyze the change of lncRNA and mRNA transcripts. Then we predicted the potential transcription factor for these significantly changed transcripts.
Project description:Anlotinib exerted cytotoxity on pancreatic cancer cells. To identify potential anlotinib targets in pancreatic cancer, we performed a microarray profiling (Affymetrix) in human PANC-1 cells treated with anlotinib.
Project description:Perineural invasion (PNI) is a unique biological feature of pancreatic cancer and is a key cause of pancreatic cancer metastasis, recurrence and poor postoperative survival, but its mechanism is largely unclarified. Clinical sample analysis and endoscopic ultrasonographic elasticity scoring indicated that cancer-associated fibroblasts (CAFs) are closely related to the occurrence of PNI. Furthermore, CAF-derived extracellular vesicles played an extremely important role in PNI in a dorsal root ganglion (DRG) coculture model and sciatic nerve model. Next, we demonstrated that CAFs promoted PNI via extracellular vesicle transmission of PNI-associated transcript (PIAT). To determine how CAF EVs exert its function, we performed mRNA sequencing on PANC-1 treated with CAFs-derived EVs
Project description:Gemcitabine has been a first-line therapeutic agent for pancreatic ductal adenocarcinoma (PDAC) pancreatic cancer; however, acquisition of resistance to gemcitabine remains a major challenge. We analyzed miRNAs expression profiles by array-based miRNAs analysis between gemcitabine–resistant (PANC-1/GEM) and parental PANC-1 cells.
Project description:Perineural invasion (PNI) is a unique biological feature of pancreatic cancer and is a key cause of pancreatic cancer metastasis, recurrence and poor postoperative survival, but its mechanism is largely unclarified. Clinical sample analysis and endoscopic ultrasonographic elasticity scoring indicated that cancer-associated fibroblasts (CAFs) are closely related to the occurrence of PNI. Furthermore, CAF-derived extracellular vesicles played an extremely important role in PNI in a dorsal root ganglion (DRG) coculture model and sciatic nerve model. Next, we demonstrated that CAFs promoted PNI via extracellular vesicle transmission of PNI-associated transcript (PIAT). To explored the potential mRNA interacted with YBX1, we we performed YBX1 RNA immunoprecipitation–sequencing (RIP-seq).
Project description:Pancreatic cancer is a fatal disease associated with resistance to conventional therapies. GLV-1h153 is an oncolytic virus which has shown promise for the targeted treatment of cancer, and is engineered to carry the human sodium iodide symporter (hNIS) for the imaging of viral replication within tumors via enhanced uptake of several radionuclide probes. We used microarrays to determine changes in gene expression patterns over time associated with infection and susceptibility of pancreatic cancer cells to GLV-1h153. Understanding into the molecular mechanisms associated with PANC-1 sensitivity to GLV-1h153 may enable identification of cancers resistant to viral therapy, avoid undesirable side effects associated with the need for higher doses of viral treatment, and development of safer and more efficacious oncolytic virotherapies. PANC-1 cells were infected with GLV-1h153. Zero (T0), 6 (T6) and 24 (T24) hours after infection, 3 samples of each time point were harvested and gene expression patterns assessed using HG-U133A cDNA microarray chips as compared to uninfected control (T0).