Project Title

Metabolic Targets of Gnaphalin Mediated Apoptosis in Colon and Pancreatic Cancer Cell Lines

Authors' Affiliations

Austin Gardner1, Samuel Ngata1, LaTravia Howard1, Caden Cox1, Anna Lee1, Danielle Eskins1, Ruben D. Torrenegra2, Oscar Rodriguez3, and Victoria E. Palau1,4

1 Bill Gatton College of Pharmacy, East Tennessee State University, Johnson City, TN 37614.
2 Departmento de Ciencias y Tecnologia, Universidad de Ciencias Aplicadas y Ambientales, Bogota,Colombia. 3 Department of Environmental Engineering, El Bosque University, Bogota, Colombia
4 Department of Internal Medicine, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614

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

Classification of First Author

Pharmacy Student

Project's Category

Biomedical and Health Sciences

Abstract Text

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.

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Apr 5th, 8:00 AM Apr 5th, 12:00 PM

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.