J Appl Biomed 12:87-95, 2014 | DOI: 10.1016/j.jab.2013.02.002

Modulatory effect of selenium on cell-cycle regulatory genes in the prostate adenocarcinoma cell line

Agnieszka Wanda Piastowska-Ciesielska^a,*, Małgorzata Gajewska^b, Waldemar Wagner^c, Kamila Domińska^a, Tomasz Ochędalski^a

^a Department of Comparative Endocrinology, Faculty of Biomedical Sciences and Postgraduate Training, Medical University of Lodz, Poland

^b Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences - SGGW, Poland

^c Laboratory of Cellular Immunology, Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland

Epidemiological data indicate that selenium status is inversely connected with cancer risk. Animal and human studies have demonstrated that most inorganic and organic forms of selenium compounds have an anticancer action. This work investigated the impact of organic selenium on the multiple signalling pathways involved in the inhibition of the viability of prostate cancer cells. Prostate adenocarcinoma cells (PC-3) were incubated with seleno-l-methionine (SeMet) at four concentrations and cell viability and programmed cell death were determined by the WST-1, BrdU assays and Tali image based cytometer. The expression of chosen cell-cycle regulatory genes was determined by real-time RT-PCR analysis and confirmed at the protein level. SeMet treatment of PC-3 cells resulted in an inhibition of cell proliferation in a dose- and time-dependent manner. The inhibition of proliferation correlated with the up-regulation of gene expression and the protein levels of CCNG1, CHEK1, CDKN1C and GADD45A, whereas SeMet down-regulated the expression of CCNA1 and CDK6 genes. Therefore SeMet inhibits the proliferative activity of prostate cancer cells by a direct influence on the expression of genes involved in the regulation of cell cycle progression.

Keywords: Selenium; Prostate; Neoplasm; Gene expression; Cells viability

Received: July 26, 2012; Revised: February 1, 2013; Accepted: February 5, 2013; Published: April 1, 2014  Show citation