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PubMed2005

Impaired nuclear translocation, nuclear matrix targeting, and intranuclear mobility of mutant androgen receptors carrying amino acid substitutions in the deoxyribonucleic acid-binding domain derived from androgen insensitivity syndrome patients.

CONTEXT: Recent imaging studies revealed that androgen receptor (AR) is ligand-dependently translocated from the cytoplasm into the nucleus and forms intranuclear fine foci. In this study, we examined whether intracellular dynamics of mutant ARs detected in two androgen insensitivity syndrome (AIS) patients was impaired. OBJECTIVE: ARs with mutations in the DNA-binding domain were functionally characterized and compared with the wild-type AR. PATIENTS: In a complete AIS patient (subject 1), cysteine residue 579 in the first zinc finger motif of AR was substituted for phenylalanine (AR-C579F). Another mutation (AR-F582Y) was found in a partial AIS patient (subject 2). RESULTS: AR-F582Y retained less than 10% of the transactivation activity of the wild-type AR, whereas no ligand-dependent transactivation was detected for AR-C579F. Image analyses of the receptors fused to green fluorescent protein showed that the wild-type AR was ligand-dependently translocated into the nucleus in which it formed fine subnuclear foci. Surprisingly, after the addition of dihydrotestosterone, the two mutant ARs initially formed large cytoplasmic dots, many of which were found to be close to mitochondria by electron microscopy. Subsequently, a part of the ligand-bound mutant ARs gradually entered the nucleus to form a smaller number of larger dots, compared with the wild-type AR. Fluorescence recovery after photobleaching analysis revealed that the intranuclear mobility of the mutant ARs decreased, compared with that of the wild-type AR. CONCLUSIONS: These results suggest that the abnormal translocation, localization, and mobility of the mutant ARs may be the cause of AIS in these subjects.

Active Transport, Cell Nucleus↗
PubMed1989

Three-month treatment with a long-acting gonadotropin-releasing hormone agonist of patients with benign prostatic hyperplasia: effects on tissue androgen concentration, 5 alpha-reductase activity and androgen receptor content.

The intraprostatic concentrations of testosterone (T) and dihydrotestosterone (DHT) have been measured in only a few men. We measured, in prostatic tissue obtained at surgery from seven men with benign prostatic hyperplasia, the effects of 3-month treatment with a long-acting GnRH agonist on 1) the intraprostatic concentrations of T, DHT, and 5 alpha-androstan-3 alpha, 17 beta-diol (3 alpha-diol); 2) prostatic 5 alpha-reductase activity; and 3) the prostatic content of androgen receptors (AR). Plasma T, DHT, and 3 alpha-diol levels also were measured. Prostatic tissue samples obtained at surgery from a group of untreated men with benign prostatic hyperplasia also were studied. The mean DHT and 3 alpha-diol concentrations in the prostatic tissue of the treated men were about 10% of those in untreated men (n = 19; P less than 0.01 for DHT and P less than 0.05 for 3 alpha-diol), and the mean intraprostatic T concentration in the treated men was about 25% of that in the control group (0.10 greater than P greater than 0.05). The mean in vitro formation of DHT by the prostatic tissue of the treated men was about 50% lower (P less than 0.05) than that by prostatic tissue of the untreated men (n = 9). The mean cytosolic AR content in the prostatic tissue of the treated men was significantly higher (P less than 0.05), whereas the mean nuclear content of both salt-extractable and salt-resistant AR was significantly lower (P less than 0.05) than that in the prostatic tissue of the untreated men (n = 8). The mean plasma T levels in treated men decreased from 4.77 +/- 1.79 (SD) ng/mL (16.5 +/- 6.2 nmol/L) to 0.27 +/- 0.42 ng/mL (0.9 +/- 1.5 nmol/L) after 1 month of therapy and remained in the castrate range thereafter. We conclude that pharmacological castration resulting from 3-month treatment with a long-acting GnRH agonist decreases the intraprostatic T concentration to about one fourth and those of DHT and 3 alpha-diol to about one tenth of the levels in untreated men. Thus, GnRH agonist treatment may not completely abolish intraprostatic androgen concentrations in metastatic prostatic cancer patients. The decrease in prostatic 5 alpha-reductase activity as well as the decrease in nuclear receptors are probably secondary to the decrease in plasma T concentrations.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1996

Different phenotypes in a family with androgen insensitivity caused by the same M780I point mutation in the androgen receptor gene.

Mutations in the coding sequence of the androgen receptor (AR) gene result in a wild range of androgen insensitivity (AI) syndromes. Differences in the clinical expression of the same mutation in unrelated patients have been reported. However, this study reports for the first time strikingly different phenotypes among three patients within the same kindred. Two of the patients had a feminine phenotype, suggesting complete AI, but for some pubic hair. The third subject was male with partial AI, perineoscrotal hypospadias, and cryptorchidism. 5 alpha-reductase activity measured in genital skin fibroblasts and binding capacity of the AR were higher in the male than in the two patients with female phenotype. Northern blot analysis of AR messenger RNA revealed a 10-kb band of normal intensity in the three subjects. Molecular analysis of the coding sequence of the AR revealed a unique M780I mutation in exon 6, changing a methionine 780 to isoleucine in the hormone-binding domain. In conclusion, the same mutation of the AR gene in the same family can result in clinical phenotypes characteristic of complete or partial AI. Therefore, the molecular defect of the AR gene may not alone predict the phenotype in families with AI.

Androgens↗
PubMed1997

Mosaicism due to a somatic mutation of the androgen receptor gene determines phenotype in androgen insensitivity syndrome.

Premature stop codons of the human androgen receptor (AR) gene are usually associated with a complete androgen insensitivity syndrome. We, however, identified an adult patient with a 46,XY karyotype carrying a premature stop codon in exon 1 of the AR gene presenting with signs of partial virilization: pubic hair Tanner stage 4 and clitoral enlargement. No other family members were affected. A point mutation at codon position 172 of the AR gene was detected that replaced the original TTA (Leu) with a premature stop codon TGA (opal). Careful examination of the sequencing gel, however, also identified a wild-type allele, indicating a mosaicism. In addition, elimination of the unique AflII recognition site induced by the mutation was incomplete, thus confirming the coexistence of mutant and wild-type AR alleles in the patient. Normal R1881 binding and a normal 110/112-kDa AR doublet in Western immunoblots consolidated the molecular genetic data by demonstrating the expression of the wild-type AR in the patient's genital skin fibroblasts. Transfection analysis revealed that only relatively high plasmid concentrations carrying the mutated AR complementary DNA lead to expression of a shortened AR due to downstream reinitiation at methionine 189. Thus, reinitiation does not play a role in the presentation of the phenotype; rather, the partial virilization is caused by the expression of the wild-type AR due to a somatic mosaic. We conclude that somatic mosaicism of the AR gene can represent a substantial factor for the individual phenotype by shifting it to a higher degree of virilization than expected from the genotype of the mutant allele alone.

Adult↗
PubMed1999

Androgen receptor-mediated hypersensitivity to androgens in women with nonhyperandrogenic hirsutism: skewing of X-chromosome inactivation.

Idiopathic hirsutism may result from an increase in the androgen receptor (AR)-mediated sensitivity of the hair follicle. The AR gene is located on the X-chromosome and contains a highly polymorphic trinucleotide repeat (CAGn) in its first exon, whose length and methylation pattern affect both AR expression and function. We analyzed these CAG repeats in the genomic DNA from 16 nonhyperandrogenic hirsute patients (Ferriman score: 16 +/- 4.7, mean +/- SD) and 10 normal controls (Ferriman score: 3 +/- 1.4), who were similar in their hormonal profiles. We found no difference in the number of CAG repeats between hirsute patients and controls, and no correlation between number of repeats and the Ferriman score or hormonal values. However, after DNA digestion with methylation-sensitive HpaII and measurement of the optical density, we found a marked decrease in the hirsute group (P < 0.0001), which was greater than in the control group (P = 0.0003). In addition, in the hirsute patients, the shorter of the two alleles was preferentially less methylated (P = 0.007), suggesting skewing of X-chromosome inactivation in the patients but not in the controls. When the mean optical density of both alleles was correlated with the Ferriman score, we observed a significant negative correlation (P = 0.02, r = -0.45), which became stronger when the shorter alleles were analyzed separately (P = 0.01; r = 0.48). We conclude that nonhyperandrogenic hirsutism is associated with skewing of X-chromosome inactivation in peripheral blood lymphocytes. This leads to the longer of the two AR alleles being preferentially methylated, allowing for the shorter (and presumably, more functional) allele to be expressed on the active X-chromosome. Further studies need to be performed to investigate whether this phenomenon is present in androgen-sensitive tissues in these patients.

Adult↗
PubMed2005

Androgen receptor mutations identified in prostate cancer and androgen insensitivity syndrome display aberrant ART-27 coactivator function.

The transcriptional activity of the androgen receptor (AR) is modulated by interactions with coregulatory molecules. It has been proposed that aberrant interactions between AR and its coregulators may contribute to diseases related to AR activity, such as prostate cancer and androgen insensitivity syndrome (AIS); however, evidence linking abnormal receptor-cofactor interactions to disease is scant. ART-27 is a recently identified AR N-terminal coactivator that is associated with AR-mediated growth inhibition. Here we analyze a number of naturally occurring AR mutations identified in prostate cancer and AIS for their ability to affect AR response to ART-27. Although the vast majority of AR mutations appeared capable of increased activation in response to ART-27, an AR mutation identified in prostate cancer (AR P340L) and AIS (AR E2K) show reduced transcriptional responses to ART-27, whereas their response to the p160 class of coactivators was not diminished. Relative to the wild-type receptor, less ART-27 protein associated with the AR E2K substitution, consistent with reduced transcriptional response. Surprisingly, more ART-27 associated with AR P340L, despite the fact that the mutation decreased transcriptional activation in response to ART-27. Our findings suggest that aberrant AR-coactivator association interferes with normal ART-27 coactivator function, resulting in suppression of AR activity, and may contribute to the pathogenesis of diseases related to alterations in AR activity, such as prostate cancer and AIS.

Amino Acid Substitution↗
PubMed2005

Complete androgen insensitivity syndrome caused by the R855H mutation in the androgen receptor gene.

Complete androgen insensitivity syndrome (CAIS) is characterized by a completely female phenotype in a 46,XY individual and is caused by mutations in the androgen receptor (AR) gene. A 5 year-old girl presented with bilateral hernia and was noted to have bilateral testes. She had a 46,XY karyotype and was diagnosed with CAIS. To identify the underlying mutation, the exons 2 to 8 of the AR gene were amplified by PCR using sets of known primers and reaction conditions. The results of the mutational analysis for the AR showed the presence of the R855H mutation; her mother was found to be heterozygous and both her 46,XX sister and her aunt had a normal AR gene. This mutation, is the result of a guanine to adenine transition in codon 855 at position 2926 in exon 7 of the AR gene, which causes an alteration of the coding nucleotide triad from CGC to CAC, which subsequently causes the substitution from arginine to histidine in the amino acid sequence of the receptor protein molecule. The same mutation has been reported to cause variable phenotypic expression, which could be explained by the presence of additional co-activating factors modifying the biological activity of the AR. The identification of an AR mutation in a girl with CAIS provides important information, because of the syndrome's genetic heterogeneity. This report emphasizes the fact that genetic determinants outside the coding sequence of the AR can influence the function of the AR protein molecule. Phenotypic expression of the mutation may be used for the construction of maps of functional domains of the AR.

Androgen-Insensitivity Syndrome↗
PubMed1999

Evidence that the CAG repeat in the androgen receptor gene is associated with the age-related decline in serum androgen levels in men.

In men over 30 years old, serum levels of testosterone (T) decrease with age. A shorter polymorphic CAG repeat length in exon 1 of the androgen receptor (AR) gene is associated with higher transcription activation by the AR. We determined the number of CAG repeats for 882 men aged between 40 and 70 years from the Massachusetts Male Aging Study (MMAS). MMAS is a population-based random sample survey of men for whom baseline (1987-1989, mean age 53+/-8 years) and follow-up (1995-1997, mean age 61+/-8 years) serum hormone levels were available. Multiple linear regression was used to determine if CAG repeat length would be predictive of hormone levels at follow-up. Hormone levels measured included T, free T, albumin-bound T, dihydrotestosterone (DHT), sex hormone-binding globulin (SHBG) and luteinizing hormone (LH). The CAG repeat length was significantly associated with T (P=0.041), albumin-bound T (P=0.025) and free T (P=0.003) when controlled for age, baseline hormone levels and anthropometrics. Follow-up levels of T decreased by 0.74%+/-0.36 per CAG repeat decrement. Likewise, the percentages of free and albumin-bound T decreased by 0.93%+/-0.31 and 0.71%+/-0.32 per CAG repeat decrement respectively. These results suggest that androgen levels may be modulated by AR genotype.

Adult↗
PubMed1998

One additional mutation at exon A amplifies thermolability of androgen receptor in a case with complete androgen insensitivity syndrome.

We have previously demonstrated a substitutional mutation (glycine to alanine at position 820) of the androgen receptor (AR) gene in a patient with complete androgen insensitivity syndrome (CAIS). We first examined whether the mutation could lead to a disorder in AR binding activity in in vitro expression experiments. In a luciferase assay, the effect of the mutant AR on a target's gene was definitely impaired. However, the mutant AR had less thermal instability compared to that of the patient's fibroblast cell lines established in a whole-cell binding assay. In order to analyze the cause of the thermal instability, a further analysis of exon A in the AR gene was performed because the previous study had been performed only between exon B and H encoding the DNA-binding domain and the hormone-binding domain. The second mutation (leucine to proline at position 257) was newly identified. In in vitro expression experiments, the AR with both mutations showed marked thermal instability, whereas the AR with a mutation in exon A had no effect on thermal stability. The results show that the N-terminal domain might also play an important role in amplifying or modifying the AR binding activity.

Androgen-Insensitivity Syndrome↗
PubMed1999

A novel E153X point mutation in the androgen receptor gene in a patient with complete androgen insensitivity syndrome.

AIM: To study a 46, XY newborn patient with a phenotype suggestive of an androgen insensitivity syndrome to confirm an anomaly in the AR gene. METHODS: Genomic DNA from leukocytes was isolated in order to analyze SRY gene by PCR and sequencing of the eight exons of AR gene. Isolation of human Leydig cell mesenchymal precursors from the testis was performed in order to study testosterone production and response to hCG stimulation in culture. RESULTS: Surgical exploration disclosed two testes, no Wolffian structures and important Müllerian derivatives. The SRY gene was present in peripheral blood leukocytes. Sequencing of the AR gene evidenced a previously unreported G to T transversion in exon 1 that changed the normal glutamine 153 codon to a stop codon. Interstitial cell cultures produced sizable amounts of testosterone and were responsive to hCG stimulation. CONCLUSION: This E153X nonsense point mutation has not been described previously in cases of AIS, and could lead to the synthesis of a short truncated (153 vs 919 residues) non functional AR probably responsible for the phenotype of complete androgen insensitivity syndrome (CAIS).

Androgen-Insensitivity Syndrome↗
PubMedDate not supplied

Androgen and androgen receptor antagonist responsive primary African-American benign prostate epithelial cell line.

The generation of suitable in vitro models is critical for understanding the process associated with the development and progression of prostate cancer in high-risk African-American men. However, the generation of long-term human prostate epithelial cell lines derived from primary human prostate epithelium have been unsuccessful due to the absence of in vitro immortalization. We have successfully established an immortal human prostate epithelial cell line from primary benign tissues of African-American prostate cancer patients by using telomerase. The actively proliferating secondary African-American prostate epithelial RC-165N cells, derived from benign prostate tissue of a radical prostatectomy specimen, were transduced through infection with a retrovirus vector expressing the human telomerase catalytic subunit (hTERT). A high level of telomerase activity was detected in RC-165N/hTERT cells but not in RC-165N cells. RC-165N/hTERT cells are currently growing well at passage 50 whereas RC-165N cells senesced within passage 3. RC-165N/hTERT cells exhibit epithelial morphology. These immortalized cells showed no cell growth in soft agar, and no tumor formation in SCID mice. The RC-165N/hTERT cells express androgen-regulated prostate-specific homobox gene. NKX 3.1 and epithelial cell specific cytokeratin 8, androgen receptor (AR), prostate stem cell antigen and p16, but not PSA. AR protein was detected by Western blot analysis.

Androgen Antagonists↗
PubMed1987

Fluorinated androgens and progestins: molecular probes for androgen and progesterone receptors with potential use in positron emission tomography.

In order to develop imaging agents for receptor-positive tumors of the breast and prostate, we have investigated the binding affinity of several fluorine-substituted steroids in the testosterone and nortestosterone series for the androgen receptor and the progesterone receptor. The 6 alpha- and 11 beta-fluoro-, and 16 alpha-fluoroalkyl-substituted steroids were prepared by an olefin bromofluorination reaction followed by dehydrobromination or reductive debromination. The 17 alpha-fluoromethyl derivatives were prepared by fluoride ion attack on the 17-spiroepoxide or 17-spiro sulfate and the 17 alpha-fluoropropynyl derivative, by reaction of a propargyl alcohol precursor with diethylaminosulfur trifluoride. Of the compounds synthesized, 17 alpha-(3-fluoro-I-propynyl)nortestosterone was found to possess the highest binding affinity and selectivity for the progesterone receptor, and 11 beta-fluoronordihydrotestosterone had the greatest affinity for the androgen receptor. Both receptor systems seem to tolerate reasonably well the substitution of fluorine for hydrogen.

Androgens↗
PubMedDate not supplied

Administration of constant low doses of androgens to steers by silastic implant. Suppression of gonadotropins and peripheral conversion of androgens.

Yearling Hereford calves approximately 300 kg in weight were castrated and assigned to one of six treatment groups receiving subcutaneous implants (3 implants, 0.5 cm diameter by 10 cm length, 10% steroid by weight) of either androstenedione (D); testosterone (T); 5 alpha-androstane-3 beta, 17 beta-diol (3 beta-diol); dihydrotestosterone (DHT); androsterone (A); or control (no steroid). Blood samples were obtained at half-hour intervals for eight hours one day prior to, and one week after, castration. The castration-induced elevation in FSH secretion was suppressed or modified by the DHT, T, and 3 beta-diol implants. LH levels were not significantly suppressed. The T implants elevated serum T concentrations; DHT implants elevated serum 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) and 3 beta-diol, but not DHT concentrations; 3 beta-diol implants elevated serum 3 beta-diol concentrations. The effects of D and A implants upon serum androgen concentrations were not statistically significant, although observations in vitro suggested an adequate release rate. These data imply that T and DHT, or metabolites of DHT, suppress FSH secretion and suggest that extensive peripheral androgen metabolism occurs.

Androgens↗
PubMed2004

Protection of androgen-dependent human prostate cancer cells from oxidative stress-induced DNA damage by overexpression of clusterin and its modulation by androgen.

BACKGROUND: Recent studies reported that oxidative stress is one of the major factors associated with the progression of prostate cancer through the accumulation of DNA damage. In the present study, we investigated the effect of oxidative stress on cell injury using androgen-dependent human prostate cancer LNCaP cells overexpressing clusterin, which has been shown to play crucial roles in the acquisition of resistance to several apoptotic stimuli. METHODS: We introduced clusterin cDNA into LNCaP cells which do not express a detectable level of clusterin expression, and generated a clusterin-overexpressing cell line (LNCaP/Cl) and a control vector only-transfected cell line (LNCaP/Co). The effects of hydrogen peroxide (H2O2) treatment on the LNCaP sublines with and without the addition of dihydrotestosterone (DHT) were analyzed using the in vitro mitogenic assay and lipid peroxidation assay, and morphological changes in the LNCaP sublines after H2O2 treatment were examined by staining with Hoechst 33258. The degrees of DNA damage induced by H2O2 into the LNCaP sublines were evaluated by the measurement of 8-hydroxy-2'-deoxyguanosine (8-OHdG) level. RESULTS: H2O2-induced apoptosis in LNCaP/Cl was significantly suppressed compared with that in LNCaP/Co through the inhibition of membrane damage; however, the measurement of 8-OHdG level demonstrated that DNA damage was more intensively accumulated in LNCaP/Cl cells than LNCaP/Co cells. Furthermore, DHT suppressed the incidence of apoptotic cell death and enhanced the formation of 8-OHdG in both LNCaP/Cl and LNCaP/Co cells after H2O2 treatment in a dose-dependent manner. CONCLUSIONS: These findings suggest that clusterin may contribute to conferring resistance to oxidative stress-mediated cellular injury on prostate cancer cells, especially in the presence of androgen.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Androgens directly stimulate mineralization and increase androgen receptors in human osteoblast-like osteosarcoma cells.

5 alpha-Dihydrotestosterone (DHT), an active form of testosterone, was shown to stimulate the mineralization of osteoblasts in a time- and dose-dependent manner in vitro in the presence of inorganic phosphate, as well as transforming growth factor beta and 1 alpha, 25 dihydroxyvitamin D3. However, DHT, stimulated the mineralization by a different mechanism from that of transforming growth factor beta and 1 alpha, 25 dihydroxyvitamin D3. We found that DHT increased the number of androgen receptors. These findings suggest that androgens directly stimulate mineralization in osteoblasts associated with an increase in the number of their receptors.

Alkaline Phosphatase↗
PubMed2000

Active allele loss of the androgen receptor gene contributes to loss of androgen receptor expression in female breast cancers.

Given the importance of androgen and androgen receptor (AR) in the control of female breast growth and the potential association with female breast cancer, we evaluated the AR expression in 114 female breast cancers and further analyzed why AR expression was lost. Immunohistochemical analysis revealed that 14.1% (17/114) of the tumors lost the AR expression completely. To unravel the molecular mechanism for AR expression loss, we first analyzed the somatic mutations in exons 2 through 8 of the AR gene by PCR-SSCP, but no mutation was detected. As the CAG repeats within exon 1 are also microsatellite markers, we then analyzed whether allelic loss was present. Interestingly, 11 of the 17 AR-negative tumors were heterozygous and 9 of them showed allelic loss. The lost allele was further demonstrated to be the active one by X-chromosome inactivation analysis. To confirm the immunohistochemical results, Northern and Western blot hybridization was performed and neither AR mRNA nor protein was detected in these AR-negative tumors. Loss of the active AR allele was strongly correlated with the AR expression loss (P = 0.0005). We conclude that AR expression loss is attributed to the active allele loss of AR gene in female breast cancers. Our finding may be also crucial in predicting and influencing the response of breast cancer to endocrine therapy.

Alleles↗
PubMed1991

Oral contraceptives, androgens, and the sexuality of young women: II. The role of androgens.

The relationships between plasma free testosterone (FT) and measures of sexual attitude, sexual behavior, and gender role behavior were assessed in 55 oral contraceptive-using and 53 nonusing female undergraduates. Plasma FT and other measures of androgenicity were substantially lower in the oral contraceptive (OC) group. Correlations between FT and certain behavioral and attitudinal measures were found in the OC users but not the nonusers. In the OC users, FT was positively associated with frequency of sexual intercourse but not with frequency of masturbation. It was negatively associated with restrictive sexual morality. Correlations between FT and measures of gender role behavior were negligible, and FT was unrelated to proceptivity, homosexual interest, or the use of sexual fantasy. The occurrence of some predicted correlations among pill-using women but not the nonusers requires explanation, particularly in view of the substantially lower levels of FT in the pill-using group. It is suggested that androgen-behavior relationships in women are easily obscured by psychosocial influences and in this sample of young women such influences may have been more powerful among those not using OCs. Such psychosocial influences are likely to differ at different stages of women's life cycles. The importance of controlling for such influences in any study of hormone-sexual behavior relationships in women is emphasized, and the need for prospective studies of women before and after starting on steroidal contraception is recognized.

Adult↗
PubMed1990

[Significance of sex hormone binding globulin and free androgen index in the estimation of androgenic cases].

Hormone analyses for hirsute women suggested that free testosterone was most revealing in biological effects and sex-hormone-binding globulin (SHBG) was quantitatively persuative. Presented in this paper are the measurements of testosterone, androstendion, dehydroepiandrosterone-sulfate (DHAS), SHBG, androstandiol and free androgen index (FAI) in 51 women with hirsutism. 92% of the hirsute women with elevated androgen level showed decrease in SHBG values and increase in FAI. 17 females with hirsutism revealed abnormally high androstandiol values which were highly related to the values of total and free testosterone (r = 0.78, r = 0.80, respectively). It is suggested that in clinical practice SHBG and FAI should also be measured besides testosterone and DHAS.

Androgens↗