Differential control of apoptosis by DJ‐1 in prostate benign and cancer cells

AbstractDJ‐1 is a conserved protein reported to be involved in diverse cellular processes ranging from cellular transformation, control of protein–RNA interaction, oxidative stress response to control of male infertility, among several others. Mutations in the human gene have been shown to be associated with an autosomal recessive, early onset Parkinson's disease (PARK7). The present study examines the control of DJ‐1 expression in prostatic benign hyperplasia (BPH‐1) and cancer (PC‐3) cell lines in which DJ‐1 abundance differs significantly. We show that while BPH‐1 cells exhibit low basal level of DJ‐1 expression, stress‐inducing agents such as H2O2 and mitomycin C markedly increase the intracellular level of the polypeptide. In contrast, DJ‐1 expression is relatively high in PC‐3 cells, and incubation with the same cytotoxic drugs does not modulate further the level of the polypeptide. In correlation with the expression of DJ‐1, both cytotoxic agents activate the apoptotic pathway in the prostatic benign cells but not in PC‐3 cells, which are resistant to their action. We further demonstrate that incubation of BPH‐1 cells with TNF‐related‐apoptosis‐inducing‐ligand/Apo‐2L (TRAIL)