Author(s)

Tomilowo Abijo^1,2*, Jiahua Xie²

¹Department of Biology, Howard University, Washington DC, USA.
²Department of Pharmaceutical Sciences, BRITE, North Carolina Central University, Durham, USA.

Selenium (Se) is a trace element required for normal body function. Its supplementation of human diet at standard optimum amount prevents oxidative damages in cells and could be a viable method in the prevention of diseases related to DNA damage, including cancer, neurodegenerative diseases and aging. While Se anticancer properties have been linked to its ability to remove excess Reactive Oxygen Species (ROS) in cells, the underlying molecular mechanism remains unknown. Recent studies have shown that the removal of ROS alone cannot account for Se anticancer properties. To really comprehend the molecular basis of Se anticancer properties, current researches now focus on the metabolism of Se in the cell, especially Se-containing amino acids. Selenocysteine (Sec) is a novel amino acid and one of the selenium-containing compounds in the cell. It is essential in the maintenance of the integrity of its parent proteins, some of which include enzymes such as Glutathione Peroxidases (GPXs) and Thioredoxin Reductases (TrXs). We propose in this study that the overproduction of Sec via the overexpression of Selenocysteine synthase (SecS) gene and Se supplementation induced cell death in Prostate Carcinoma (PC-3) cells. Although the mechanism underlying the cell death induction is unknown, we propose it could be due to the random incorporation of Sec into proteins at high concentration, causing premature protein degradation and cell death. The outcome of this study showed that increasing the concentration of intracellular Se-containing amino acids may provide important clinical implications for the treatment of cancer.

Selenium, Reactive Oxygen Species, Selenocysteine, Prostate Carcinoma, Selenocysteine Synthase Gene

Abijo, T. and Xie, J. (2016) Preliminary Study of Selenium (Se) Toxicity in Human Prostate Carcinoma (PC3) Cells with the Overexpression of Selenocysteine Synthase (SecS) Gene. Open Journal of Genetics, 6, 79-86. doi: 10.4236/ojgen.2016.64009.