Androgen Regulation of c-myc Messenger Ribonucleic Acid Levels in Rat Ventral Prostate

Abstract

Androgens regulate growth of the rat ventral prostate gland. In a search for possible mediators of androgen stimulated growth we have studied c-myc proto-oncogene expression in ventral prostate after androgen withdrawal and replacement. Steady state levels of c-myc mRNA were determined by Northern hybridization and compared with mRNA levels for prostatein, the major androgen dependent protein of ventral prostate. C-myc mRNA in ventral prostate increased nearly 4-fold within 1 day and 6- to 7-fold within 2 days after castration. Administration of androgen at the time of castration prevented this increase in c-myc mRNA levels. Androgen treatment of 4-day castrate rats caused c-myc mRNA levels to decrease within 4 h. Cycloheximide increased c-myc mRNA severalfold within 2 h. The net increase in c-myc mRNA after cycloheximide treatment was greater in the castrate than in the noncastrate or in androgen-treated castrate rats. These results suggest that androgen may influence both transcription and turnover of c-myc mRNA. Prostatein C3 mRNA decreased rapidly after castration and increased after androgen treatment of the castrate but was only slightly influenced by cycloheximide. Steady state levels of c-myc mRNA were higher in the 10-day-old rat and decreased with age while prostatein C3 mRNA increased with age. In situ hybridization demonstrated that both c-myc and prostatein mRNAs are expressed in the epithelial cells of ventral prostate acinar glands. These data indicate that androgens regulate the expression of c-myc in the ventral prostate.

Modulation of rat preadipocyte adipose conversion by androgenic status: involvement of C/EBPs transcription factors

“…On the other hand, in various cell types and tissues, c-myc expression has been shown to be regulated by sex-steroid hormones (Schuchard et al 1993). For example, testosterone treatment reduces c-myc mRNA level, in vivo, in the rat ventral prostate (Quarmby et al 1987) and, in vitro, in human prostatic cells (Wolf et al 1992).…”

Association of castration-dependent early induction of c-myc expression with a cell proliferation of the ventral prostate gland in rat

“…A transient increase of c-myc mRNA occurs during liver regeneration after a partial hepatectomy (Makino et al, 1984) and also has been demonstrated after mitogenic stimulation of quiescent lymphocytes (Kelly et al, 1983). Conversely, c-myc mRNA was increased in the involution of the prostate after castration in rat, and the induction of c-myc mRNA was correlated with apoptosis of the ventral prostate (Quamby et al, 1987). Recently, Lee et al reported that c-myc mRNA is transiently induced at the beginning of a period after castration (Lee et al, 1999).…”

“…Late induction of c-myc mRNA may play a role in the epithelial cell regression and apoptosis was seen in the ventral prostate after androgen withdrawal (Quamby et al, 1987). To investigate whether an early induction of c-myc mRNA is related to apoptosis, DNA fragmentation was assayed.…”

“…Castration-induced death of prostatic epithelial cells is accompanied by specific gene expression, i.e. c-myc (Quamby et al, 1987;Buttyan et al, 1988), p53 (Colombel et al, 1992), and IGFBP (Nickerson et al, 1998). c-Myc protooncogene appears to play an important role in the regulation of cell growth.…”

FLIP-ping out: Death receptor signaling in the prostate

“…First, c-myc mRNA levels increase following castration, as shown by multiple groups. [141][142][143] This might seem paradoxical, given the well-known role of c-myc in cell proliferation. However, it is now quite clear that c-myc can drive apoptosis under conditions where other proliferative signals (such as IGF-1) are absent or reduced.…”