Dietary
selenium intake has been linked to reduced
cancer risk, however the underlying mechanisms are yet unknown. We question the commonly used practice of applying
selenium concentrations found in human blood to in vitro studies and evaluated the utility of
biomarkers, e.g.,
glutathione peroxidase 1 (GPx1) and
thioredoxin reductase 1 (TrxR1), to determine appropriate
selenium levels for in vitro work. Furthermore, we investigated the effects of
Se-methylselenocysteine (SeMSC) on
prostate cancer cell migration and invasion. After excluding cytotoxicity, we demonstrated that
prostate cancer cell lines respond differently to
selenium treatment as observed through
biomarker assessment. We found that the maximum levels of GPx1 activity and TrxR1 expression were reached at lower
selenium concentrations in LNCaP compared to PC3 cells, and PC3 compared to DU145 cells. Therefore the use of
selenium concentrations extrapolated from human studies for in vitro work may be applicable when further informed using a readout of
selenium repletion including use of
selenium responsive
biomarkers. No effect on PC3 migration or invasion was observed after long term SeMSC treatment; however a slight increase was found when treatment was solely administered during the assay. The opposite could be observed when cells were cultured under low serum conditions, with a significant increase in migration upon long term but not upon acute SeMSC treatment. To conclude, these findings indicate that it is imperative to study the
selenium sensitivity of an in vitro model preferably using
biomarkers before investigating any effects on biological processes, or before comparing models.