Investigating the anti-cancer activities of the Delta-Tocotrienols and Gamma-Tocopherols on Prostate cancer cells in combination.
TOCOTRIENOLS CAN SUPPORT
INDUCTION OF APOPTOSIS IN PROSTATE CANCER CELLS
CELL CYCLE ARREST IN THE G1 AND G2/M PHASE
INHIBITION OF PROSTATE CANCER CELL GROWTH
Introduction to Prostate Cancer and TRFProstate cancers are caused when the cells of the prostate gland start to multiply uncontrollably. Prostate cancer is the 2nd leading cause of cancer-related deaths in the United States. In this study, a combination of Delta-Tocotrienols, and Gamma-Tocopherols was investigated for their anticancer properties against prostate cancer cells. Hence, in this study it has been investigated if the combination of both the isomers strengthens the inhibitory effects Delta-Tocotrienols on prostate cancer cell growth.
How does Delta-Tocotrienol fight Prostate Cancer?In this study, the activities of Annatto Delta-Tocotrienols and Gamma-Tocopherol were investigated against the human androgen-dependent prostate cancer cells (LNCaP). It was observed that the combined treatment of Gamma-Tocopherol and Delta-Tocotrienol resulted in reinforced anti-prostate cancer mechanisms and activities. The combination of both the isomers induced G1 arrest as well as G2/M arrest. The combined treatment also resulted in enhanced induction of apoptosis or programmed cell death in the prostate cancer cells. Hence, it can be concluded from the study that the combination of Gamma-Tocopherol and Delta-Tocotrienol incredibly inhibits the growth of prostate cancer cells due to the simultaneous cell cycle arrest in the G1 as well as the G2/m phase.
To conclude, Tocotrienols have been observed to have high potential in the prevention and treatment of prostate cancer. In vitro studies have shown that Gamma-Tocotrienols promotes apoptosis and autophagy in human prostate cancer cells. Moreover, Tocotrienol rich fraction (TRF) has also displayed chemopreventive and therapeutic activities against prostate cancer cells by inducing cell cycle arrest and apoptosis.
Reference for the Study in detail:1. https://pubmed.ncbi.nlm.nih.gov/29225320/
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