Project description:By studying a mouse model, as well as human tumors samples and cell lines, we have revealed a tumor suppressive role for Gata6 in the pathogenesis of pancreatic ductal adenocarcinoma (PDAC). In order to understand the mechanism underlying such tumor suppressive function, we analyzed the genome-wide DNA-binding of GATA6 in a human PDAC cell line (PaTu8988S). GATA6 is found to bind the promoter of genes involved in the epithelial differentiation programme, as well as of genes involved in the mesenchymal programme. With this we describe a novel GATA6-dependent mechanism of regulation of EMT. Examination of GATA6 binding to the DNA in a human PDAC cell line
Project description:FASTQ Sequencing files of 5 healthy pancreas tissues and 6 pancreatic ductal adenocarcinoma (PDAC) tissues. Analysis of data is presented in the manuscript: Next generation sequencing reveals novel differentially regulated mRNAs, lncRNAs, miRNAs, sdRNAs and a piRNA in pancreatic cancer in BMC Molecular Cancer.
Project description:Aberrant expression of truncated O-glycan structures, such as Tn and STn, is frequently observed in pancreatic ductal adenocarcinoma (PDAC). The focus of our study is to investigate the functional role of truncated O-glycans in PDAC progression and metastasis. Our study revealed that kmockout of C1GALT1 leads to increased expression of truncated glycans and accelerates PDAC progression and metastasis.
Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest digestive system malignancies; its incidence is increasing and it is predicted to be the second most common cause of death within the next decade. Recent studies demonstrated the increased tendency of LN metastasis in PDAC. Yet the biological role and underlying regulatory mechanism of hsa_circ_0060665 in lymph node (LN) metastasis of PDAC remain unclear. Our study aims to explore the target genes of hsa_circ_0060665 and the underlying mechanism in the LN metastasis of PDAC.
Project description:Pancreatic adenocarcinoma (PDAC) is one of the most lethal human malignancies and a major health problem. Patient-derived xenografts (PDX) are appearing as a prime approach for preclinical studies despite being insufficiently characterized as a model of the human disease and its diversity. We generated subcutaneous PDX from PDAC samples obtained either surgically or using diagnostic biopsies (endoscopic ultrasound guided fine needle aspirate). The extensive multiomics characterization of the xenografts demonstrated that PDX is a suitable model for preclinical studies, representing the diversity of the primary cancers. We generated subcutaneous PDX from PDAC samples obtained either surgically or using diagnostic biopsies (endoscopic ultrasound guided fine needle aspirate). The variable 'MultiOmicsClassification' indicates the resulting sample's group. 'CIMPclass' is the CpG island methylator phenotype as estimated from the methylation arrays analysis. In this dataset, Illumina Infinium HumanCode-24 BeadChips SNP arrays were used to analyze the DNA xenografts samples from pancreatic ductal adenocarcinoma.
Project description:Little is known about the role of FOXO3 and PDHA1 in PDAC. We performed microarrays to revealed the transcriptional change of a human pancreatic ductal adenocarcinoma (PDCA) cell line (Panc -1) to scr-siRNA, FOXO3-siRNA and PDHA1-siRNA in order to provide insight into the role of PDHA1 and FOXO3 in Panc-1 cells.
Project description:To further development of our lncRNA and mRNA expression approach to pancreatic ductal adenocarcinoma(PDAC), we have employed lncRNA and mRNA microarray expression profiling as a discovery platform to identify lncRNA and mRNA expression in pancreatic ductal adenocarcinoma.Human pancreatic ductal adenocarcinoma tissues and normal pancreatic tissues from PDAC donors and other duodenum diseases donors. analyze mRNA and lncRNA expression in pancreatic ductal adenocarcinoma (PDAC) by microarray platform
Project description:Background/Aims: Microarray-based comparative genomic hybridisation (CGH) has allowed high-resolution analysis of DNA copy number alterations across the entire cancer genome. Recent advances in bioinformatics tools enable us to perform a robust and highly sensitive analysis of array CGH data and facilitate the discovery of novel cancer-related genes. Methods: We analysed a total of 29 pancreatic ductal adenocarcinoma (PDAC) samples (six cell lines and 23 microdissected tissue specimens) using 1 Mb-spaced CGH arrays. The transcript levels of all genes within the identified regions of genetic alterations were then screened using our Pancreatic Expression Database. Results: In addition to 238 high-level amplifications and 35 homozygous deletions, we identified 315 minimal common regions of “non-random” genetic alterations (115 gains and 200 losses) which were consistently observed across our tumour samples. The small size of these aberrations (median size of 880 kb) contributed to the reduced number of candidate genes included (on average 12 Ensembl-annotated genes). The database has further specified the genes whose expression levels are consistent with their copy number status. Such genes were UQCRB, SQLE, DDEF1, SLA, ERICH1 and DLC1, indicating that these may be potential target candidates within regions of aberrations. Conclusion: This study has revealed multiple novel regions that may indicate the locations of oncogenes or tumour suppressor genes in PDAC. Using the database, we provide a list of novel target genes whose altered DNA copy numbers could lead to significant changes in transcript levels in PDAC. (Harada et al. Pancreatology) Keywords: pancreatic ductal adenocarcinima, tissue microdissection, array CGH, genetic alterations A panel of 23 microdissected PDAC tissues and 6 PDAC-derived cell lines were analysed using Sanger's CGH arrays with 1 Mb resolution. Clinical info of the samples used is provided as a supplementary file.
Project description:Little is known about the role of FOXO3 and PDHA1 in PDAC. We performed microarrays to revealed the transcriptional change of a human pancreatic ductal adenocarcinoma (PDCA) cell line (Panc -1) to scr-siRNA, FOXO3-siRNA and PDHA1-siRNA in order to provide insight into the role of PDHA1 and FOXO3 in Panc-1 cells. Panc-1 Human PDCA cells were treated with scr-siRNA, FOXO3-siRNA and PDHA1-siRNA for 48 h and total RNA was extracted by using TRIzol Reagent. The microarray analysis was conducted on the Panc-1 cells expressing by using Agilent Microarray.