Affiliations: [a] Department of Anatomy, Physiology and Genetics, and Institute for Molecular Medicine, Uniformed Services University of Health Sciences (USUHS) School of Medicine, Bethesda, MD, USA | [b] Pharmaceutical Genomics Division, The Translational Genomics Research Institute, Phoenix, AZ, USA | [c] Center for Prostate Disease Research, Department of Surgery, Uniformed Services University of Health Sciences (USUHS) School of Medicine, Bethesda, MD, USA
Correspondence:
[*]
Address correspondence to: Ximena Leighton, M.D., Department of Anatomy, Physiology and Genetics, USU School of Medicine, 4301 Jones Bridge Road, Bethesda. MD 20814, USA. Tel.: +1 301 295 9379; Fax: +1 301 295 1786; E-mail: xleighton@usuhs.mil.
Abstract: Evaluation of gene expression profiles in CWR22 prostate tumor xenografts in nude mice revealed overexpression of the Cytochrome b561, a transmembrane electron transport protein abundant in neuroendocrine vesicles, in the castration recurrent prostate cancers (CRPC). Four fold higher levels of the Cytochrome b561 was present in highly metastatic and androgen refractory LNCaP/C4-2 prostate cancer cells in comparison to androgen responsive and non-metastatic LNCaP cells. In LNCaP cells, Cytochrome b561 expression was induced by the synthetic androgen, R1881. Of note, Cytochrome b561 expression pattern correlated with known androgen regulated genes in epithelial transcriptome of primary prostate tumors. Taken together, these novel findings suggest that the expression of Cytochrome b561, is androgen regulated in the context of CaP cells and its increased expression in CRPC reflects increased androgen receptor signaling in tumor cells. These observations warrant further evaluation of functions and biomarker potential of Cytochrome b561 in CRPC.
