Hdl Handle:
http://hdl.handle.net/10675.2/601938
Title:
Effectors Implicated In the Ac1 Inhibitory Effect on Cell Proliferation in Pancreatic Cancer Cells
Authors:
Medepalli, Vidya
Abstract:
Introduction and aim: Pancreatic adenocarcinoma is among the most aggressive of all cancers. Adenosine 3’, 5’ cyclic monophosphate (cyclic AMP) is involved in the internal cellular enzymatic activity and gene expression. It is found to be involved in the mechanism of pancreatic tumorigenesis. So far, two effectors for cyclic AMP are known; one is protein kinase A (PKA) and the other is an exchange protein directly activated by cAMP (EPAC). Our research group has found that AC1 is responsible for the inhibitory effect of Forskolin on cell proliferation of HPAC. My research project focuses on studying the effectors implicated in the inhibitory effect of activated AC1. Result: We were successfully able to overexpress AC1 using a plasmid human ADCY1 cDNA in pCMV-SPORT6. Through the overexpression, we were able to support the conclusion that AC1 inhibits cell proliferation in HPAC cells. We found that both H-89 (inhibitor of PKA) and ESI (inhibitor of EPAC) counteracts the effect of AC1. Conclusion: Both effectors- PKA and EPAC- mediate the inhibitory effect of AC1. Funding Source: Center for Undergraduate Research and Scholarship and Department of Biological Sciences, Scholarly Activity Award
Affiliation:
Department of Biological Sciences
Issue Date:
Mar-2016
URI:
http://hdl.handle.net/10675.2/601938
Type:
Presentation
Language:
en_US
Description:
Presentation given at the 17th Annual Phi Kappa Phi Student Research and Fine Arts Conference
Appears in Collections:
17th Annual Phi Kappa Phi Student Research and Fine Arts Conference: Oral Symposia I

Full metadata record

DC FieldValue Language
dc.contributor.authorMedepalli, Vidyaen
dc.date.accessioned2016-03-17T12:59:36Zen
dc.date.available2016-03-17T12:59:36Zen
dc.date.issued2016-03en
dc.identifier.urihttp://hdl.handle.net/10675.2/601938en
dc.descriptionPresentation given at the 17th Annual Phi Kappa Phi Student Research and Fine Arts Conferenceen
dc.description.abstractIntroduction and aim: Pancreatic adenocarcinoma is among the most aggressive of all cancers. Adenosine 3’, 5’ cyclic monophosphate (cyclic AMP) is involved in the internal cellular enzymatic activity and gene expression. It is found to be involved in the mechanism of pancreatic tumorigenesis. So far, two effectors for cyclic AMP are known; one is protein kinase A (PKA) and the other is an exchange protein directly activated by cAMP (EPAC). Our research group has found that AC1 is responsible for the inhibitory effect of Forskolin on cell proliferation of HPAC. My research project focuses on studying the effectors implicated in the inhibitory effect of activated AC1. Result: We were successfully able to overexpress AC1 using a plasmid human ADCY1 cDNA in pCMV-SPORT6. Through the overexpression, we were able to support the conclusion that AC1 inhibits cell proliferation in HPAC cells. We found that both H-89 (inhibitor of PKA) and ESI (inhibitor of EPAC) counteracts the effect of AC1. Conclusion: Both effectors- PKA and EPAC- mediate the inhibitory effect of AC1. Funding Source: Center for Undergraduate Research and Scholarship and Department of Biological Sciences, Scholarly Activity Awarden
dc.language.isoen_USen
dc.subjectPancreatic Neoplasmsen
dc.subjectAdenocarcinomaen
dc.subjectPlasmidsen
dc.titleEffectors Implicated In the Ac1 Inhibitory Effect on Cell Proliferation in Pancreatic Cancer Cellsen_US
dc.typePresentationen
dc.contributor.departmentDepartment of Biological Sciencesen
dc.description.advisorSabbatini, Mariaen
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