Effects of 40H-tamoxifen on the proliferation and apoptosis of prostate stromal cells.
- Author:
Yi-Ming FU
1
;
Qiu-Ming LI
;
Chun-Ying ZHANG
;
Zhao-Yan CHEN
;
Cheng-Luo JIN
;
Yun-Hui CHAN
;
Min-Kai WU
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents, Hormonal; pharmacology; Apoptosis; drug effects; Cell Proliferation; drug effects; Cell Survival; drug effects; Cells, Cultured; Dose-Response Relationship, Drug; Humans; Male; Prostate; cytology; Stromal Cells; cytology; drug effects; Tamoxifen; pharmacology
- From: National Journal of Andrology 2007;13(7):620-623
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of 4OH-Tamoxifen (OHT) on proliferation and apoptosis of primary cultured prostate stromal cells.
METHODSPrimarily cultured prostate stromal cells in vitro were treated with various concentrations (10(-8) mol/L - 10(-5) mol/L) of estradiol (E2), diethylstilbestrol (DES), OHT and the mixture of E2 (10(-8) mol/L - 10(-6) mol/L) with OHT (10(-7) mol/L) and then MTT and TUNEL were used to detect their proliferation and apoptosis respectively.
RESULTSThere was a significant difference (P < 0.05) between OHT and estrogens in the effects on the apoptosis and proliferation of the primarily cultured prostate stromal cells. OHT suppressed proliferation of the prostate stromal cells at the concentrations from 10(-7) mol/L to 10(-5) mol/L (P < 0.05), and this effect was concentration related (r = -0.383, P = 0.005); OHT (10(-7) mol/L) suppressed the proliferation stimulation effect of E2 at the concentrations from 10(-8) mol/L to 10(-6) mol/L (P < 0.05). OHT induced apoptosis at the concentrations from 10(-8) mol/L to 10(-5) mol/L (P < 0.05), and this effect was concentration related (r = 0.349, P = 0.012). The apoptosis induced by OHT could not be reversed by E2 at the concentrations from 10(-8) mol/L to 10(-5) mol/L (P > 0.05).
CONCLUSIONOHT can obviously suppressed the proliferation and promote the apoptosis of primarily cultured prostate stromal cells, which might not be totally attributed to the competitive inhibition of the estrogen receptor.
