Browsing 18th Annual PKP Student Research and Fine Arts Conference: Posters by Subjects
Now showing items 1-2 of 2
The Structural and Functional Properties of a Splice Variant of ADCY7 Gene in Human Pancreatic CancerAlternative splicing of mRNA precursors is a regulated process of gene expression in eukaryotic cells. It provides cells with the opportunity to create protein isoforms of different functions from a single gene. Cancer cells often take advantage of this process to produce proteins that promote growth and survival. Cyclic adenosine monophosphate (cyclic AMP) is a second messenger that has shown to suppress migration and invasion of pancreatic ductal adenocarcinoma cells. Cyclic AMP is formed from cytosolic ATP by the enzyme adenylyl cyclase (AC). There are ten isoforms of ACs; nine are anchored in the plasma membrane and one is soluble. Our goal was to find alternative splice variants of transmembrane AC isoforms in pancreatic cancer. We found a possible splice variant of type VII adenylyl cyclase (ADCY7) in human healthy pancreatic, adjacent non-tumor, tumor tissues, two pancreatic cancer cell lines HPAC and PANC-1, epithelial duct cell line PDEC, but not in isolated human pancreatic acini (the exocrine part of the pancreas). Further research will be carried out to study the structural and functional properties of the splice variant of human ADCY7.
Structural, Kinetic and Functional Properties of CAP1/AC ComplexesThe major cause of death in pancreatic cancer is due to metastases; therefore, it is important to study the mechanism by which the pancreatic cancer cells migrate and invade. This would help advance therapeutics and ultimately help prolong survival. Adenylyl cyclase-associated protein 1 (CAP1) is a scaffold protein that is involved in the regulation of actin microfilament formation, which ultimately leads to cell migration and invasion. CAP1 binds to G-actin inhibiting polymerization. We first tested whether CAP1 binds to adenylyl cyclase (AC) by performing co-immunoprecipitation. We found that CAP1 not only interacts with G-actin, but also with a number of AC isoforms: AC1, AC3, AC4 and AC7. Further studies need to be done to determine how CAP1/AC/G-actin interact and the impact of these interactions on the invasive behavior of pancreatic cancer cells.