Development and evaluation of canine reference genes for accurate quantification of gene expression.
BACKGROUND Retinoic acid (RA) is recognized as an inhibitor of tumorigenesis, but conversely, has also been shown to act as a tumor enhancer, therefore its role in prostate tumor cell growth was investigated. METHODS The response of two human prostate tumor cell lines (PC-3 and DU-145), and cell lines derived from a well-differentiated canine prostate adenocarcinoma (CPA) and normal canine prostate epithelium (CAPE) to all-trans RA was determined using growth curve analysis. Additionally, the constitutive expression and RA-challenged expression of retinoic acid receptors (RARs) -alpha, -beta, and -gamma mRNA was examined using Northern blotting techniques. RESULTS In response to all-trans RA, the PC-3 and DU-145 cell lines showed considerable growth promotion, while CAPE and CPA cell growth was dramatically inhibited. Each cell line expressed RAR alpha and RAR gamma, with either negligible or no RAR beta transcripts being detected. RAR alpha and -gamma mRNAs detected in the four cell lines were variably regulated in response to RA, and no distinct patterns of RAR regulation that could be related to cell growth responses were observed. CONCLUSIONS The data indicates that no simple association exists between the expression or regulation of RAR subtype mRNAs and the divergent growth responses to RA displayed by the prostate cell lines.