Cloning of cDNAs encoding the α and β subunits of rat casein kinase 2 (CK-2): Investigation of molecular regulation of CK-2 by androgens in rat ventral prostate

Casein kinase 2 (CK-2) is a ubiquitous messenger-independent protein serine/threonine kinase that has been implicated in the control of cell growth and proliferation. By employing androgen action in the prostate as a model of growth control, we have previously documented that androgens modulate prostatic CK-2 activity in a tissue specific manner. Here we have investigated the role of transcriptional control of prostatic CK-2 in androgenic regulation of its activity. We first cloned and sequenced full length cDNAs encoding the α and β subunits of rat CK-2. The cDNA sequence encoding the α subunit corresponded with previously reported sequences for other species, as well as with the derived partial amino acid sequence reported for a rat cDNA. The cloned cDNA for rat CK-2-β subunit, not reported previously, was also identical in amino acid sequence to that of other species. The cDNAs for α and β subunits were employed as probes to examine the effects of altered androgenic status on transcription of mRNAs for the subunits of prostatic CK-2. Androgen deprivation caused a slow decline in transcription of the a subunit, so that no change was noted at 24 h postcastration; however, at later periods of androgen deprivation a progressive but relatively slow decline was apparent. Administration of a single dose of 5α-dihydrotestosterone (5α-DHT) to 6-d castrated animals did not elicit an early expression of new mRNAs for CK-2-α and β subunits. However, a significant expression of mRNAs for the two subunits was apparent at 8 h (i.e., later stages of the prereplicative phase) reaching a peak in the proliferative phase of prostatic growth (i.e., at 24-48 h) following androgen administration. These data suggest that androgenic regulation of CK-2 gene transcription is not an early event related to androgen action, but is substantial in the prereplicative phase of prostatic cell proliferation mediated by androgen. Further, androgenic stimulation of the mRNA expression for the α and β subunits of CK-2 appears to be differential.