Metabolic Targets of Gnaphalin Mediated Apoptosis in Colon and Pancreatic Cancer Cell Lines
Location
Ballroom
Start Date
4-5-2018 8:00 AM
End Date
4-5-2018 12:00 PM
Poster Number
95
Name of Project's Faculty Sponsor
Dr. Victoria Palau
Faculty Sponsor's Department
Department of Internal Medicine, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614
Type
Poster: Competitive
Project's Category
Biomedical and Health Sciences
Abstract or Artist's Statement
Colorectal and pancreatic cancer are leading causes of cancer related mortality, suggesting the need for further development of treatment approaches. Gnaphalin, a flavone derived from Gnaphalium gracile H. B. K. which is found in the Andean regions of South America, has shown anti-proliferative properties in solid tumors. Further investigation has shown this compound interferes with signaling conducive to proliferation and cell adhesion, inducing the cell to undergo apoptosis. The primary objective of the study was to look at key regulatory proteins in the cell survival and proliferative pathways to determine Gnaphalin’s mechanism of action. Cytotoxic activity was measured using MTT analysis on the colon cancer cell lines Caco2 and HCT-116, and on the pancreatic cancer cell lines MIA PaCa and Panc28. Apoptosis was determined by the presence of fragmented DNA via TUNEL and cleaved effector caspase 3. Finally, immunoblots were used to determine the mechanism of action using key proteins involved in both the intrinsic and extrinsic apoptotic pathways. Gnaphalin showed the highest activities in colon cancer HCT-116 and pancreatic cancer Panc 28 cells with a half maximal effective concentrations of 25.82±1.0887 and 30.07 ± 1.553 µM respectively. Gnaphalin impediment of cell viability involves the inhibition of phospho-ERK proliferation of the MAPK pathway along with phospho-FAK and c-Met, which are adhesion molecules. Gnaphalin has shown cytotoxic activity towards several colon cancer and pancreatic cancer cell lines by targeting cell proliferation and adhesion, and ultimately causing apoptosis.
Metabolic Targets of Gnaphalin Mediated Apoptosis in Colon and Pancreatic Cancer Cell Lines
Ballroom
Colorectal and pancreatic cancer are leading causes of cancer related mortality, suggesting the need for further development of treatment approaches. Gnaphalin, a flavone derived from Gnaphalium gracile H. B. K. which is found in the Andean regions of South America, has shown anti-proliferative properties in solid tumors. Further investigation has shown this compound interferes with signaling conducive to proliferation and cell adhesion, inducing the cell to undergo apoptosis. The primary objective of the study was to look at key regulatory proteins in the cell survival and proliferative pathways to determine Gnaphalin’s mechanism of action. Cytotoxic activity was measured using MTT analysis on the colon cancer cell lines Caco2 and HCT-116, and on the pancreatic cancer cell lines MIA PaCa and Panc28. Apoptosis was determined by the presence of fragmented DNA via TUNEL and cleaved effector caspase 3. Finally, immunoblots were used to determine the mechanism of action using key proteins involved in both the intrinsic and extrinsic apoptotic pathways. Gnaphalin showed the highest activities in colon cancer HCT-116 and pancreatic cancer Panc 28 cells with a half maximal effective concentrations of 25.82±1.0887 and 30.07 ± 1.553 µM respectively. Gnaphalin impediment of cell viability involves the inhibition of phospho-ERK proliferation of the MAPK pathway along with phospho-FAK and c-Met, which are adhesion molecules. Gnaphalin has shown cytotoxic activity towards several colon cancer and pancreatic cancer cell lines by targeting cell proliferation and adhesion, and ultimately causing apoptosis.