For this purpose, the androgen receptor (AR) expressing human breast cancer cell line T47D was stably transfected with a luciferase gene under transcriptional control of the PB-ARE-2 androgen response element.
Breast cancer is a rare disease in men.Germ-line mutations in BRCA2 and androgen receptor (AR) genes are thought to be responsible for a proportion of male breast cancer cases.
More recently, AR allele length was also inversely correlated with the histological grade of breast cancer, but no association was found between the AR-CAG polymorphism and the risk of either breast or ovary cancer.
A previous study has suggested that BRCA1 carriers with longer lengths of the CAG repeat in the androgen receptor (AR) gene are at increased risk of breast cancer (BC).
Every breast cancer cell line exhibited a distinct expression pattern of the nuclear receptor co-regulators examined raising the possibility that the relative levels of these co-activators/-repressors might differentially modulate androgen receptor transcriptional activity within the promoter/enhancer region of KLK2 and KLK3 of these cells.
In the presented study, we have analysed effects of the environmental estrogens bisphenol A (BPA), p-tert-octylphenol (OCT), o,p'-DDT (DDT) and coumestrol (COU) on cell proliferation, apoptosis induction, progesterone receptor (PR) and androgen receptor (AR) mRNA expression and ER alpha protein expression in comparison to estradiol (E2) and the selective ER modulator (SERM) raloxifene (RAL) and the pure antiestrogen faslodex (ICI 182780) in the human breast cancer cell line MCF-7.
In order to define AR in breast cancer, 67 primary breast tumours and 8 normal breast samples as control tissue were analysed for AR expression at the mRNA and protein levels using RT-PCR and Western blotting, respectively.
Because AR coactivators enhance transactivation of AR, in this report we evaluated the relationship of a CAG/CAA repeat length polymorphism in the AIB1/SRC-3 gene (amplified in breast cancer gene 1, a steroid receptor coactivator and an AR coactivator) with prostate cancer risk in a population-based case-control study in China.
The AR CAG repeat among patients with early onset (<42 years) breast cancer was significantly shorter (17.5+/-2.3) compared with asymptomatic individuals (18.6+/-2.1) (P<0.01), and the shorter allele - the younger the age at diagnosis.
Women diagnosed with breast cancer before age 45 years and age-matched controls, all participants in a population-based case-control study of breast cancer, were assessed for length variation in the (CAG)(n) and (GGC)(n) AR repeats within the AR gene.
Hormonal therapies in prostate and breast cancer that directly target AR and ERalpha, respectively, are then presented and possible novel drug targets in the SHR pathway are discussed.
AR-mediated effects of these synthetic progestins were studied in an in vitro transactivation assay, employing DNA co-transfection of an AR expression vector and luciferase reporter gene construct in the MDA-MB 231 human breast cancer cell line.
Overexpression of androgen receptor (AR) decreases estrogen receptor alpha (ERalpha) transactivation, which plays a basic role in hormone-dependent breast cancer.
It appears that androgen receptor status may influence the effect of selenium on gene expression profile in prostate cancer; whether estrogen receptor may influence the effect of selenium on gene expression in breast cancer requires further studies.