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dc.contributor.authorMedepalli, Vidya
dc.date.accessioned2017-03-06T18:38:02Z
dc.date.available2017-03-06T18:38:02Z
dc.date.issued2017-03
dc.identifier.urihttp://hdl.handle.net/10675.2/621296
dc.descriptionPresentation given at the 18th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractPancreatic adenocarcinoma is among the most aggressive of all cancers in the United States. Cyclic adenosine monophosphate (cyclic AMP) is a second messenger that regulates the proliferation and migration of pancreatic cancer cells. Cyclic AMP is formed from cytosolic ATP by the enzyme adenylyl cyclase (AC). In the presence of forskolin, a transmembrane AC activator, the proliferation and migration of pancreatic cells have been inhibited. Since the mechanisms underlying the inhibitory effect of activated adenylyl cyclase are little understood, we investigated the downstream mediators implicated in the AC/cyclic AMP pathway. With this purpose, we overexpressed AC1 in the human pancreatic adenocarcinoma (HPAC) cell line, and through the protein kinase A (PKA) inhibitor H-89 and the exchange protein directly activated by cyclic AMP (EPAC) inhibitor ESI-09, we assessed the effector involved upon the treatment with forskolin. In a previous study, we showed that PKA alone mediates the inhibitory effect of forskolin/AC1/cyclic AMP on proliferation of HPAC cells. In the present study, we examined the effectors implicated in the AC1 inhibitory effect on cell migration through utilization of the CytoSelect 24-well cell migration assay kit. Our current experimental data suggests that PKA and EPAC are both likely to be downstream mediators in the effect of forskolin/AC1/cyclic AMP on migration of HPAC cells.
dc.language.isoenen
dc.subjectAdenocarcinomaen
dc.subjectPancreatic Neoplasmsen
dc.subjectAdenylyl Cyclasesen
dc.subjectCell Movementen
dc.titleEffectors Implicated in the Adenylyl Cyclase 1 Inhibitory Effect on Cell Migration in Pancreatic Cancer Cellsen
dc.typePresentationen
dc.contributor.departmentDepartment of Biologic Sciencesen
dc.description.advisorSabbatini, Mariaen
refterms.dateFOA2019-04-10T08:21:58Z
html.description.abstractPancreatic adenocarcinoma is among the most aggressive of all cancers in the United States. Cyclic adenosine monophosphate (cyclic AMP) is a second messenger that regulates the proliferation and migration of pancreatic cancer cells. Cyclic AMP is formed from cytosolic ATP by the enzyme adenylyl cyclase (AC). In the presence of forskolin, a transmembrane AC activator, the proliferation and migration of pancreatic cells have been inhibited. Since the mechanisms underlying the inhibitory effect of activated adenylyl cyclase are little understood, we investigated the downstream mediators implicated in the AC/cyclic AMP pathway. With this purpose, we overexpressed AC1 in the human pancreatic adenocarcinoma (HPAC) cell line, and through the protein kinase A (PKA) inhibitor H-89 and the exchange protein directly activated by cyclic AMP (EPAC) inhibitor ESI-09, we assessed the effector involved upon the treatment with forskolin. In a previous study, we showed that PKA alone mediates the inhibitory effect of forskolin/AC1/cyclic AMP on proliferation of HPAC cells. In the present study, we examined the effectors implicated in the AC1 inhibitory effect on cell migration through utilization of the CytoSelect 24-well cell migration assay kit. Our current experimental data suggests that PKA and EPAC are both likely to be downstream mediators in the effect of forskolin/AC1/cyclic AMP on migration of HPAC cells.


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