Inhibition of cultured rat prostatic epithelial cell growth by epristeride in vitro
Abstract
Aim: To study the molecular mechanism of rat prostate atrophy induced by epristeride.
Methods: MTT test was used to determine the effect of epristeride on the growth of prostatic epithelial cell induced by exogenous epithelial growth factor (EGF) or insulin-like growth factor-I (IGF-I). RT-PCR and flow cytometry were then used to quantitatively detect the mRNA and protein expressions of EGFR and IGF-I R of the epithelial cells treated or untreated with epristeride.
Results: Epristeride attenuated growth of epithelial cells induced by exogenous EGF, IGF-I. Epristeride 360 nmol/L inhibited EGFR and IGF-I R expression at mRNA level, while epristeride 180 nmol/L had no marked effect on EGFR and IGF-I R mRNA expression. Both epristeride 180 nmol/L and 360 nmol/L could down regulate EGFR and IGF-I R protein levels.
Conclusion: The molecular mechanisms of prostatic epithelial cell atrophy induced by epristeride might be associated with alteration in the expression of growth factor receptors such as EGF and IGF-I.
Keywords:
Methods: MTT test was used to determine the effect of epristeride on the growth of prostatic epithelial cell induced by exogenous epithelial growth factor (EGF) or insulin-like growth factor-I (IGF-I). RT-PCR and flow cytometry were then used to quantitatively detect the mRNA and protein expressions of EGFR and IGF-I R of the epithelial cells treated or untreated with epristeride.
Results: Epristeride attenuated growth of epithelial cells induced by exogenous EGF, IGF-I. Epristeride 360 nmol/L inhibited EGFR and IGF-I R expression at mRNA level, while epristeride 180 nmol/L had no marked effect on EGFR and IGF-I R mRNA expression. Both epristeride 180 nmol/L and 360 nmol/L could down regulate EGFR and IGF-I R protein levels.
Conclusion: The molecular mechanisms of prostatic epithelial cell atrophy induced by epristeride might be associated with alteration in the expression of growth factor receptors such as EGF and IGF-I.