| Autor: |
Bjerknes C; Hofseth Biocare, Kipervikgata 13, 6003 Ålesund, Norway., Framroze B; Hofseth Biocare, Kipervikgata 13, 6003 Ålesund, Norway.; GPH Biotech LLC, 1455 Adams Drive, Menlo Park, CA 94025, USA., Currie C; Hofseth Biocare, Kipervikgata 13, 6003 Ålesund, Norway., Pettersen CHH; Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, 7491 Trondheim, Norway., Axcrona K; Department of Urology, Akershus University Hospital, 1478 Lørenskog, Norway., Hermansen E; Hofseth Biocare, Kipervikgata 13, 6003 Ålesund, Norway.; Department of Clinical Medicine, University of Bergen, 5007 Bergen, Norway. |
| Abstrakt: |
Prostate cancer is a common cause of cancer death in men. In advanced stages of prostate cancer, androgen deprivation therapy (ADT) is initiated. Despite ADT, prostate cancers invariably progress to become androgen independent. A growing body of evidence implicates iron dysmetabolism in prostate cancer progression. A bioactive peptide-rich salmon protein hydrolysate (SPH) has previously been demonstrated to modulate iron homeostatic mechanisms. In the present study, the anticancer effect of SPH and bicalutamide co-treatment on LNCaP and PC3 prostate cancer cell proliferation was investigated. Our results found that SPH potentiates the anti-proliferative effect of bicalutamide in a dose-dependent manner for both cell lines. In the presence of 160 µg/mL SPH, co-treatment with 1.0 µM bicalutamide decreased LNCaP cells' relative colony survival from 25% (1.0 µM bicalutamide monotreatment) to 2% after culturing for 12 days. For PC3 cells, the relative colony survival diminished from 52% (10.0 µM bicalutamide) to 32% at an SPH concentration of 160 µg/mL. Gene expression profiling, employing quantitative real-time PCR, revealed that the inhibitory effects were related to significant FTH1 up-regulation with a concomitant TFRC down-regulation. In conclusion, our results provide in vitro evidence that SPH potentiates the growth inhibitory effect of bicalutamide on prostate cancer cells by modulating iron homeostasis mechanisms. |
