Androgen-responsive and -unresponsive prostate cancer cell lines respond differently to stimuli inducing neuroendocrine differentiation.

摘要: The treatment of advanced prostate cancer (CaP) with androgen deprivation therapy inevitably renders the tumours castration resistant and incurable. Under these conditions, neuroendocrine differentiation (NED) CaP cells occurs neuropeptides released by facilitate tumour progression. Pharmacological strategies aiming to prevent or delay NED during ablation could, therefore, increase effectiveness therapy. Mechanisms pathways inducing in are poorly understood data often discordant. In present study, we used several cell lines (androgen-responsive: LNCaP, PC3-AR, 22RV1 -irresponsive: DU145 PC3) evaluate after epidermal growth factor (EGF). was determined neuron-specific enolase chromogranin A expression occurrence morphological changes cells. Androgen-deprivation conditions induced LNCaP but not 22Rv1, PC3 PC3-AR also became thapsigargin-induced apoptosis. all AR-positive lines, caused a decrease receptor indicating that it is downregulated irrespective induction. Treatment EGF inhibitor gefinitib prevented process. On contrary, no effect demonstrated 22Rv1 did respond univocally treatments NED, suggesting studies on this topic should be performed wide spectrum models which can more indicative variability vivo.