Project description:Pancreatic ductal adenocarcinoma, caused by activating mutation in K-Ras, is an aggressive malignancy due to its early invasion and matastasis. Ral GTPases, negatively regulated by RalGAP, are activated downstream of Ras and play a crucial role in development and progression of pancreatic ductal adenocarcinoma. However, the underlying mechanisms remain unclear. We used microarrays to detail the global programme of gene expression underlying the human pancreatic ductal adenocarcinoma cell line, MIA PaCa-2 with RalGAPβ deficiency or not, and identified distinct classes of Ral activation-related mRNA.
Project description:Transcriptional profiling of Mia PaCa 2 cells treated with 5-Aza for 96 h. Relative abundance to untreated control cells was used to estimate the effect of DNA demethylation on the expression of the RNAs. Two-condition experiment, 5-Aza-treated vs. untretated Mia PaCa 2 cells. Biological replicates: 2. Technical replicates: 2.
Project description:Endogenous LYSET/TMEM251 was isolated via Co-IP from MIA PaCa-2 cells. LYSET KO cells were used as controls. Cells were grown in SILAC medium for 3 passages
Project description:To investigate the impact of the mRNA stabilty factor HuR on the pancreatic cancer transcriptome in MIA PaCa-2 in vitro cell line and in vivo tumors at multiple time points of tumor growth
Project description:Glucose metabolism makes contributions to the development of pancreatic ductal adenocarcinoma (PDAC). Meanwhile, circular RNAs, a subset of noncoding RNAs, plays an important role in glucose metabolism and cancer progression. Analysis of low-glucose-treated and normal-glucose-treated MIA PaCa-2 cells from 6 samples (3 samples each group) was conducted. Results indicate insight into molecular signature of the pathogenesis of PDAC in abberant glucose metabolism.