Project description:TNFα-producing Macrophages Determine Subtype Identity and Prognosis via AP1 Enhancer Reprogramming in Pancreatic Cancer [cJUN-OE RNA-seq]
Project description:TNFα-producing Macrophages Determine Subtype Identity and Prognosis via AP1 Enhancer Reprogramming in Pancreatic Cancer [TNFa-treatment RNA-seq]
Project description:In pancreatic cancer, classical and basal-like subtypes are identified as two major PDAC subtypes. Our previous data showed that PDAC tumor cells can switch between the two phenotypes through transcriptional reprogramming particularly in response to inflammatory cues. In this study, we were trying to understand TNFα mediated transcription regulatory network in pancreatic cancer. Hence, we performed RNA-seq in TNFα treated classical cells as well as aqua dest control.
Project description:In pancreatic cancer, two distinct transcriptomic subtypes were identified with a high prognostic relevance: the classical and basal-like subtype. Therefore, in this study, we wanted to use an unbiased method to investigate the global chromatin accessibility in subtype-defined pancreatic cancer cell lines, as well as define the binding profile of the highly subtype-dependent JUN/AP1 transcription factors JUNB (classical) and cJUN (basal). Hence, we performed ATAC-seq in two classical and basal-like cells, as well as ChIP-seq for JUNB in classical CAPAN1 cells and for cJUN in basal-like PANC1 cells.
Project description:According to our previous data, BRD4 controls the inflammatory cJUN transcription factor via enhancer interaction to promote a basal-like phenotype in pancreatic cancer. Therefore, in this study, we wanted to asses BRD4-mediated 3D chromatin interactions at a potential cJUN enhancer locus in pancreatic cancer. Hence, we performed i4C-seq in PANC1 cells in absencece and presence of the BET/BRD4 inhibitor JQ1 for this site.
Project description:According to our previous data, it shows that cJUN plays an important role in regulating inflammation and basal-like phenotype in pancreatic cancer. Therefore, in this study, we wanted to use an unbiased method to investigate the global effect of cJUN in pancreatic cancer. Hence, we performed RNA-seq in GCDX62-EV cells, as well as GCDX62-cJUN cells