Project description:Evaluation of interaction frequency in parental L3.6pl cells, paclitaxel-resistant cells and resistant cells treated with a CDK9 inhibitor
Project description:Pancreatic adenocarcinoma (PDAC) is a lethal disease and it is the most common type of pancreatic cancer. Majority of the pancreatic cancers harbor alterations in the Kras gene. Currently there are no approved drugs that target Kras directly and it's downstream effect on the epigenome remains unknown. In this study, we investigated the epigenetic landscape of pancreatic cancer cells which harbor the inducible KrasG12D allele. We performed RNA-seq, ChIP-seq against 6 different histone marks, ATAC-seq and RRBS to assess the changes in the epigenome after oncogenic KrasG12D induction.
Project description:Investigation of gene expression profile changes upon down regulation of p63 in L3.6pl and BxPC-3 cell lines which are representative of the squamous molecular subtype in pancreatic cancer
Project description:In order to investigate the funcational and mechanistic role of ARID1A in regulating PDAC development and progression, we generated mRNA expression profiles from human pancreatic cancer cell line L3.6pl, which underwent ARID1A-depletion by CRISPR-Cas9 technology. The same-processed L3.6pl parental cell line was used as control.
Project description:Pancreatic adenocarcinoma (PDAC) is a lethal disease and it is the most common type of pancreatic cancer. Majority of the pancreatic cancers harbor alterations in the Kras gene. Currently there are no approved drugs that target Kras directly and it's downstream effect on the epigenome remains unknown. In this study, we investigated the epigenetic landscape of pancreatic cancer cells which harbor the inducible KrasG12D allele. We performed RNA-seq, ChIP-seq against 6 different histone marks, ATAC-seq and RRBS to assess the changes in the epigenome after oncogenic KrasG12D induction.
Project description:Pancreatic adenocarcinoma (PDAC) is a lethal disease and it is the most common type of pancreatic cancer. Majority of the pancreatic cancers harbor alterations in the Kras gene. Currently there are no approved drugs that target Kras directly and it's downstream effect on the epigenome remains unknown. In this study, we investigated the epigenetic landscape of pancreatic cancer cells which harbor the inducible KrasG12D allele. We performed RNA-seq, ChIP-seq against 6 different histone marks, ATAC-seq and RRBS to assess the changes in the epigenome after oncogenic KrasG12D induction.
Project description:Increasing evidence suggests that defective RNA processing contributes to the development of amyotrophic lateral sclerosis (ALS). This may be especially true for ALS caused by a repeat expansion in C9orf72 (c9ALS), in which the accumulation of RNA foci and dipeptide-repeat proteins are expected to modify RNA metabolism. We report extensive alternative splicing (AS) and alternative polyadenylation (APA) defects in the cerebellum of c9ALS cases (8,224 AS, 1,437 APA), including changes in ALS-associated genes (e.g. ATXN2 and FUS), and cases of sporadic ALS (sALS; 2,229 AS, 716 APA). Furthermore, hnRNPH and other RNA-binding proteins are predicted as potential regulators of cassette exon AS events for both c9ALS and sALS. Co-expression and gene-association network analyses of gene expression and AS data revealed divergent pathways associated with c9ALS and sALS. Examination transcriptiome profiles in c9orf72-associated ALS, sporadic ALS and healthy control