Abstract
Phycocyanin is a pigmented protein found in cyanobacteria produced by aphanizomenon flos-aquae (a freshwater species of blue-green algae) and spirulina. Phycocyanin (PC) has been researched extensively in the last twenty years because of its anti-cancer properties. Despite numerous critical findings, the anti-cancer mechanism for how PC induces apoptosis in cancer cells is still unknown.
The purpose of our experiment was to determine the uptake of PC by cancer cells and then study different mechanisms of apoptosis. PC naturally emits red florescence, which was utilized to verify the uptake by LNCaP prostate cancer cells. We were able to determine that PC only binds to the cell membrane; therefore we suspected that PC must interact with a membrane protein for inducing apoptosis. Since apoptosis mechanisms are regulated by an anti-apoptosis protein Bcl-2, we examined the effect of PC treatment on Bcl-2 levels. Electrophoretic separation of proteins from the LNCaP cells and a western blot analysis showed PC down regulated Bcl-2. Topotecan (TPT) an anti-cancer drug was used as a positive control to down-regulate Bcl-2 levels in A549 lung cancer cells. The combination of both PC and TPT resulted in greater down regulation of Bcl-2 that might be triggering apoptosis in cancer cells. Understanding the complete mechanism inducing apoptosis is critical for PC to be considered as a possible complimentary agent during cancer treatment. (This project was supported by the Ester-King Biomedical research program of the state of Florida).
Faculty Sponsors
Dr. Mark Jaffe
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-4-2014 1:00 PM
End Date
4-4-2014 5:30 PM
Mechanism of Apoptosis Induced by Phycocyanin in LNCaP and A549 Cancer Cells
Alvin Sherman Library
Phycocyanin is a pigmented protein found in cyanobacteria produced by aphanizomenon flos-aquae (a freshwater species of blue-green algae) and spirulina. Phycocyanin (PC) has been researched extensively in the last twenty years because of its anti-cancer properties. Despite numerous critical findings, the anti-cancer mechanism for how PC induces apoptosis in cancer cells is still unknown.
The purpose of our experiment was to determine the uptake of PC by cancer cells and then study different mechanisms of apoptosis. PC naturally emits red florescence, which was utilized to verify the uptake by LNCaP prostate cancer cells. We were able to determine that PC only binds to the cell membrane; therefore we suspected that PC must interact with a membrane protein for inducing apoptosis. Since apoptosis mechanisms are regulated by an anti-apoptosis protein Bcl-2, we examined the effect of PC treatment on Bcl-2 levels. Electrophoretic separation of proteins from the LNCaP cells and a western blot analysis showed PC down regulated Bcl-2. Topotecan (TPT) an anti-cancer drug was used as a positive control to down-regulate Bcl-2 levels in A549 lung cancer cells. The combination of both PC and TPT resulted in greater down regulation of Bcl-2 that might be triggering apoptosis in cancer cells. Understanding the complete mechanism inducing apoptosis is critical for PC to be considered as a possible complimentary agent during cancer treatment. (This project was supported by the Ester-King Biomedical research program of the state of Florida).
