Redox-sensitive protein targets of selenium in prostate cancer prevention

Raghu Sinha, Ph.D.
Biochemistry and Molecular Biology
Penn State College of Medicine, Hershey, PA 17033

Co-Authors:
Nicole D. Facompre, Biochemistry and Molecular Biology, Penn State College of Medicine, Hershey, PA 17033
John T. Pinto, Ph.D., Molecular Neurobiology, Cornell-Burke Medical Research Institute, White Plains, NY, 10605
John E. Baatz, Ph.D., Pediatrics, Medical University of South Carolina, Charleston, SC 29425
Dhimant Desai, Ph.D., Pharmacology, Penn State College of Medicine, Hershey, PA 17033
Karam El-Bayoumy, Ph.D., Biochemistry and Molecular Biology, Penn State College of Medicine, Hershey, PA 17033

ABSTRACT:
Experimental and epidemiological data support that selenium is effective in reducing the risk of prostate cancer. We hypothesize that naturally occurring organoselenium compounds such as selenomethionine (SM) and synthetic compounds such as 1,4-phenylenebis(methylene)selenocyanate (p-XSC) target redox-sensitive signal proteins thereby regulating the proliferative and / or apoptotic responses. Comparing the two-dimensional electrophoretic profiles of AR+ and AR- LNCaP cell supernatant fractions, following 24 hr treatment with SM and p-XSC revealed several differentially expressed protein spots including; cofilin-2, a muscle specific pro-apoptotic protein. SM treatment of AR- LNCaP cells induces cofilin-2 in a dose-dependent manner concurring with our hypothesis.