title: Androgen regulation of cell adhesion molecule gene expression in rat prostate during organ degeneration. C-CAM belongs to a class of androgen-repressed genes associated with enriched stem/amplifying cell population after prolonged castration.
abstract: Androgen is required for maintaining the differentiated state of prostatic epithelium, and that cell adhesion molecules play active roles in controlling the development of epithelial cells. However, little is known about the regulation of cell adhesion molecules during prostate development. In this study, we demonstrated that the expression of an epithelial cell adhesion molecule, C-CAM, in rat ventral prostatic epithelium are repressed by androgen. A similar regulatory pattern was also observed in the seminal vesicle but not in other androgen-dependent organs (the coagulating gland and the dorsolateral prostate), or other organs (the liver and kidney). These observations suggest that regulation of C-CAM expression by androgen is tissue-specific. Unlike the other androgen-repressed genes associated with apoptosis, which have transient expression patterns, the elevated level of C-CAM in the ventral prostate persisted for more than 30 days postcastration, suggesting that C-CAM belongs to a class of androgen-repressed genes which are not associated with apoptosis. Immunohistochemical study detected C-CAM on the apical surface of secretory epithelium in control rats; castration resulted in an altered localization of C-CAM expression from columnar epithelium to cuboidal basal epithelium. Taken together, the up-regulation and altered expression pattern of C-CAM in ventral prostatic epithelium by androgen deprivation may be associated with the enriched epithelial stem/amplifying cell population in degenerated ventral prostate. These observations suggest that C-CAM may play an active role in the process of prostatic epithelial differentiation.
authors.affiliation: Department of Urology, University of Texas M.D. Anderson Cancer Center, Houston 77030.
authors.forename: J T
authors.initials: JT
authors.lastname: Hsieh
authors.forename: S H
authors.initials: SH
authors.lastname: Lin
mesh_terms: D000251:Adenosine Triphosphatases; D000726:Androgen Antagonists / Q000494:pharmacology; D000818:Animals; D015703:Antigens, CD; D017209:Apoptosis; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis*; D002454:Cell Differentiation; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D005485:Flutamide / Q000031:analogs & derivatives / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009919:Orchiectomy; D009928:Organ Specificity; D011467:Prostate / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012669:Seminal Vesicles / Q000187:drug effects / Q000378:metabolism; D013739:Testosterone / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D000726:Androgen Antagonists; D015703:Antigens, CD; C069847:CD66 antigens; D015815:Cell Adhesion Molecules; C014290:hydroxyflutamide; D013739:Testosterone; D004958:Estradiol; D005485:Flutamide; D000251:Adenosine Triphosphatases