Official websites use. Share sensitive information only on official, secure websites. Dysregulation of many apoptotic related genes and androgens are critical in the development, progression, and treatment of prostate cancer. Our previous results led to the hypothesis that downregulation of TRAIL-decoy receptor DcR2 expression following androgen deprivation would leave hormone sensitive normal prostate cells vulnerable to the cell death signal generated by TRAIL via its pro-apoptotic receptors.
We tested this hypothesis under pathological conditions by exploring the regulation of TRAIL-induced apoptosis related to their death and decoy receptor expression, as also to hormonal concentrations in androgen-sensitive human prostate cancer, LNCaP, cells. The data support the hypothesis that hormone modulation of DcR2 expression regulates TRAIL-induced apoptosis in LNCaP cells, giving insight into cell death induction in apoptosis-resistant hormone-sensitive tumour cells from prostate cancer.
Prostate cancer is the most commonly diagnosed malignancy in the male population and remains the second leading cause of cancer-related deaths in the developed world [ 1 ]. Inhibition of apoptosis is a critical pathophysiological factor that contributes to the onset and progression of prostate cancer, but the molecular mechanisms are not entirely understood.
Therefore, insight into the mechanism s of the misregulation of apoptosis could be the basis for developing more effective therapeutic approaches to destroy apoptosis-resistant tumour cells, as found in prostate cancer [ 2 ]. TRAIL may therefore be a promising candidate for cancer treatment. DcR1 is a glycosylphosphatidylinositol GPI -linked protein lacking an intracellular domain, and DcR2 contains a truncated death domain.
Moreover, Clancy et al. Finally, osteoprotegerin, a regulator of osteoclastogenesis, appears to be a soluble receptor for TRAIL [ 18 ]. The idea of targeting specific death receptors to induce apoptosis in tumours is attractive; thus it is particularly intriguing to explore how a complex family of death and decoy receptors modulates TRAIL function.
