Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 382, Issue 1, Pages 314-324Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2013.10.022
Keywords
Prostate cancer; (R)-bicalutamide; MtDNA; Hormone-resistance; Mitochondrial fission
Categories
Funding
- Italian Association for Cancer Research (A.I.R.C.) [IG 11520]
- Italian Ministry for University and Scientific Research [2010NFEB9L_002]
Ask authors/readers for more resources
Advanced prostate cancers, initially sensitive to androgen deprivation therapy, frequently progress to the castration-resistant prostate cancer phenotype (CRPC) through mechanisms not yet fully understood. In this study we investigated mitochondria] involvement in the establishment of refractoriness to hormone therapy. Two human prostate cancer cell lines were used, the parental LNCaP and the resistant LNCaPRbic, the latter generated after continuous exposure to 20 RM of (R)-bicalutamide, the active enantiomer of Casodex. We observed a significant decrease in mtDNA content and a lower expression of 8 mitochondria-encoded gene transcripts involved in respiratory chain complexes in both cell lines. We also found that (R)-bicalutamide differentially modulated dynamin-related protein (Drp-1) expression in LNCaP and LNCaP-Rbic cells. These data seem to indicate that the androgen-independent phenotype in our experimental model was due, at least in part, to alterations in mitochondrial dynamics and to a breakdown in the Drp-1-mediated mitochondrial network. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available