Project description:The purpose of this study is to understand the differential gene expression analysis in p53 knockdown human SU.86.86 pancreatic cancer cells
Project description:The p53 transcription factor is a critical barrier to pancreatic cancer progression. To unravel mechanisms of p53-mediated tumor suppression, we analyzed pancreatic cancer predisposition in mice expressing p53 transactivation domain (TAD) mutants. Surprisingly, we observed that p53 TAD2 mutant behaves as a “super-tumor suppressor”, with an enhanced capacity to suppress pancreatic cancer and to activate a subset of novel p53 target genes. One such gene, Ptpn14, is a direct p53-inducible gene encoding a negative regulator of the Yap oncoprotein. To determine the effects of p53 deficiency on Yap target gene expression in pre-malignant mouse pancreatic intraepithelial neoplasia (PanIN) lesions, we sorted the CD133-positive ductal epithelial cells that make up the PanINs and used these cells for RNA-sequencing analysis. This analysis revealed that a Yap signature is induced upon p53 deficiency, suggesting that p53 loss promotes the induction of a Yap transcriptional program.
Project description:Gene expression in SU-DIPG20, SU-DIPG31, SU-DIPG35, and SU-DIPG-48 primary samples was quantified to gain insight into diffuse glioma biology.
Project description:Gene expression profile of p53 knockdown MSCs or p53 knockdown+TERT MSCs was compared with that of control MSCs. Our data show p53 knockdown prolongs the lifespan of MSCs, and a combination of p53 knockdown and TERT overexpression is sufficient to immortalize MSCs. The results provide important information about the molecular basis underlying p53 knockdown in MSCs and immortalization-related genes of MSCs. Total RNA obtained from p53 knockdown MSCs or p53 knockdown+TERT MSCs from three patients were compared with control MSCs.
Project description:Gene expression profile of p53 knockdown MSCs or p53 knockdown+TERT MSCs was compared with that of control MSCs. Our data show p53 knockdown prolongs the lifespan of MSCs, and a combination of p53 knockdown and TERT overexpression is sufficient to immortalize MSCs. The results provide important information about the molecular basis underlying p53 knockdown in MSCs and immortalization-related genes of MSCs.
Project description:SU-DHL-5 cells display limited expression of the SUMO isopeptidase SENP6. In this experiment, the chromatin associated fraction of SU-DHL-5 cells was analysed by mass spectrometry. SU-DHL-5 cells were either stably transfected with an empty vector or with a SENP6 expression construct. Changes in protein levels were compared between these two cell lines in triplicate experiments.
Project description:Gene expression levels were determined with control or MCT4 knockdown pancreatic cancer cells. MiaPaca2, Capan-2, and PL45 cells were transfected with non-specific or MCT4-specific RNAi. RNA was harvested at 72 hours post transfection and analyzed on Illumina microarrays.