Abstract
Apoptosis (programmed cell death) can be stimulated when a cell has reached its pre-determined lifespan. The intrinsic pathway is typically activated for cell cycle regulation, thus preventing tumor formation. Bcl-2 family proteins can play a pro or anti-apoptotic role by regulating the expression levels and modes of action of other proteins such as caspases, which cleave cell parts until the cell is no longer functional. Many studies are focusing on proteins that regulate the apoptotic pathway, as anomalies may lead to tumor formation. The purpose of this study was to assess effects of a novel water-soluble cancer drug, known as JFD-WS, on the intrinsic apoptotic pathway in human breast adenocarcinoma xenograft implanted athymic nude mice. JFD-WS was compared to Sutent, a control drug that is currently used as an anti-cancer treatment. It was hypothesized that JFD-WS would down-regulate anti-apoptotic proteins such as Bcl-2 and up-regulate pro-apoptotic proteins such as p53, Bax, and Apaf-1. Western blot analysis showed significant upregulation of of the aforementioned pro-apoptotic proteins, along with downregulation of the anti-apoptotic protein Bcl-2. The release of cytochrome C found in the cytosolic fraction was significantly higher in JFD-WS treated animals as compared to untreated controls. Induction of apoptosis in the JFD-WS treated group was confirmed by the presence of cleaved caspase-3. JFD-WS treatment induced apoptosis as shown by the presence of DNA fragments; thus results confirmed the proapoptotic effects of JFD-WS in human breast adenocarcinoma xenograft implanted athymic nude mice.
Faculty Sponsors
Appu Rathinavelu, Ph.D., Deanne Roopnarine, D.P.M.
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-10-2015 1:00 PM
End Date
4-10-2015 5:30 PM
Induction of Apoptosis by JFD-WS in Human Breast Adenocarcinoma Xenograft Implanted Athymic Nude Mice
Alvin Sherman Library
Apoptosis (programmed cell death) can be stimulated when a cell has reached its pre-determined lifespan. The intrinsic pathway is typically activated for cell cycle regulation, thus preventing tumor formation. Bcl-2 family proteins can play a pro or anti-apoptotic role by regulating the expression levels and modes of action of other proteins such as caspases, which cleave cell parts until the cell is no longer functional. Many studies are focusing on proteins that regulate the apoptotic pathway, as anomalies may lead to tumor formation. The purpose of this study was to assess effects of a novel water-soluble cancer drug, known as JFD-WS, on the intrinsic apoptotic pathway in human breast adenocarcinoma xenograft implanted athymic nude mice. JFD-WS was compared to Sutent, a control drug that is currently used as an anti-cancer treatment. It was hypothesized that JFD-WS would down-regulate anti-apoptotic proteins such as Bcl-2 and up-regulate pro-apoptotic proteins such as p53, Bax, and Apaf-1. Western blot analysis showed significant upregulation of of the aforementioned pro-apoptotic proteins, along with downregulation of the anti-apoptotic protein Bcl-2. The release of cytochrome C found in the cytosolic fraction was significantly higher in JFD-WS treated animals as compared to untreated controls. Induction of apoptosis in the JFD-WS treated group was confirmed by the presence of cleaved caspase-3. JFD-WS treatment induced apoptosis as shown by the presence of DNA fragments; thus results confirmed the proapoptotic effects of JFD-WS in human breast adenocarcinoma xenograft implanted athymic nude mice.
