Disease relevance of Aig1

• PMEPA1 was originally identified as a highly androgen-induced gene by serial analysis of gene expression in androgen-treated LNCaP prostate cancer (CaP) cells [1].
• Both metabolites, in a dose-dependent manner, target AR to the nucleus and inhibit androgen-induced transactivation mediated by the mouse mammary tumor virus promoter [2].
• The DDT1 MF2 smooth muscle tumor cell line was derived from an estrogen/androgen-induced leiomyosarcoma that arose in the ductus deferens of a Syrian hamster [3].
• These results indicate that androgens directly affect macrophage function in males after trauma and hemorrhagic shock and that the intracellular conversion of testosterone to dihydrotestosterone is of particular importance in mediating the androgen-induced effects [4].
• Characterization of beta-adrenergic receptor subtypes in androgen-induced mouse kidney hypertrophy using a new high-affinity ligand, [125I]iodocyanopindolol [5].

High impact information on Aig1

• In the androgen-induced destruction of the mammary rudiments of 14 day male mouse fetuses, the hormone acts directly only on the mesenchyme, which then condenses around the epithelial gland buds and--in some unknown way--causes their necrosis [6].
• However, androgen-induced declines in circulating HDL-C should not automatically be assumed to be proatherogenic, because these declines may instead reflect accelerated reverse cholesterol transport [7].
• Thus, it is clear that the androgen-induced growth of SC-3 cells is mediated in an autocrine manner by AIGF, which is secreted by the tumor cells themselves in response to hormonal stimuli [8].
• To identify the regulatory mechanism(s) underlying this strain variation in Adh-1 transcription in the B6 and B6.S kidney, liver, and androgen-induced kidney [9].
• Androgen-induced differentiation and tumorigenicity of human prostate epithelial cells [10].

Chemical compound and disease context of Aig1

• Inhibition of histone deacetylation augments dihydrotestosterone induction of androgen receptor levels: an explanation for trichostatin A effects on androgen-induced chromatin remodeling and transcription of the mouse mammary tumor virus promoter [11].

Biological context of Aig1

• These results indicate that androgen-induced FGF-like factor acts as an autocrine growth factor via the FGF receptor in a process of SC-3 cell proliferation [12].
• These results are suggestive of the significant role played by hyaluronan-CD44 interactions in mediating androgen-induced prostatic growth and morphogenesis [13].
• In the presence of dihydrotestosterone (50 nM), M2 (0.2-10 microM) inhibits androgen-induced AR binding to androgen response element DNA [2].
• Our results indicate that androgens decrease plasma adiponectin and that androgen-induced hypoadiponectinemia may be related to the high risks of insulin resistance and atherosclerosis in men [14].
• Basic fibroblast growth factor (bFGF) stimulated basal and androgen-induced growth of F614B16 cells in serum-free and serum-supplemented media, whereas it inhibited RAG cell growth [15].

Anatomical context of Aig1

• Since it was reported that the growth of cells from SC 115 was regulated by an androgen-induced fibroblast growth factor (FGF)-like peptide (1), the present study was aimed at examining whether a similar growth factor was secreted by CS 2 cells in the absence of testosterone [16].
• In these AR-null nude male mice, the androgen-stimulated growth of normal adult prostatic epithelial cells did not occur (i.e., androgen-induced growth response of normal prostatic epithelial cells requires stromal cell paracrine involvement) [17].
• The relationship between growth factor responses and androgen-induced cell proliferation was studied in a mouse renal tumor (RAG) cell line, a hybrid (F614B16) rat prostate x RAG cell line, and an 8-azaguanine-resistant revertant of the F614B16 cell line [15].
• Inhibitory effects of transforming growth factor-beta 1 on androgen-induced development of neonatal mouse seminal vesicles in vitro [18].
• Our results emphasize the importance of organ-specific fibroblasts that promote tumor growth and mediate androgen-induced growth responses; the accelerated growth of the bladder epithelium was not accompanied by the expression of PSA, a known differentiated gene product produced by human prostatic epithelial cells [19].

Associations of Aig1 with chemical compounds

• Growth-stimulatory effect of androgen-induced autocrine growth factor(s) secreted from Shionogi carcinoma 115 cells on androgen-unresponsive cancer cells in a paracrine mechanism [20].
• Interaction of androgen-induced autocrine heparin-binding growth factor with fibroblast growth factor receptor on androgen-dependent Shionogi carcinoma 115 cells [12].
• In the present study, therefore, we investigated the effect of dexamethasone on androgen-induced growth of SC115 cells in vivo and in cell culture [21].
• When androgen-induced cell proliferation was labeled with [125I]IdUrd, the incorporated radioactivity was retained in mice given continuous TP injections but not in mice given continuous TP injections but not in mice given 17 beta-estradiol (E2) or vehicle [22].
• A role for heparan sulfate in androgen-induced deoxyribonucleic acid synthesis of mouse mammary carcinoma (Shionogi carcinoma 115)-derived SC-3 cells [23].

Regulatory relationships of Aig1

• Furthermore, the highly purified growth factor-, basic FGF- or androgen-induced growth of SC-3 cells was significantly and similarly inhibited by anti-basic FGF antibody IgG [12].
• In addition, androgen-induced enhancement of DNA synthesis in SC-3 cells can be blocked by simultaneous incubation with AIGF antisense oligonucleotides [24].
• Our data suggest that a down-regulation of AP1 activities induced by epithelial cell differentiation is a prerequisite to androgen-induced mvdp gene expression [25].
• EGF also induced cell proliferation of the fetal reproductive tract in a dose-dependent manner and a combination of physiological dosages of EGF and androgen-induced cell proliferation synergistically, suggesting an interactive effect of these two drugs [26].

Other interactions of Aig1

• Down-regulation of AP1 activities after polarization of vas deferens epithelial cells correlates with androgen-induced gene expression [25].
• EGF, however, produced striking enhancement of the androgen-induced transcriptional activity when used with androgen [27].
• In support of the coordinate nature of this regulation, androgen-induced upregulation of lipogenic gene expression is accompanied by an increase in the nuclear content of SREBP, a key lipogenic transcription factor [28].
• This variation does not correlate with variation at Mup-a, a locus that controls the ratio of the three MUPs in urine from androgen-induced mice [29].
• The androgen-induced proliferation of S115 mouse mammary tumor cells has been suggested to involve autocrinic fibroblast growth factor signaling [30].

Analytical, diagnostic and therapeutic context of Aig1

• In UGM plus BLE recombinants, androgen-induced [3H]thymidine or [35S]-methionine uptake analyzed by two-dimensional gel electrophoresis was qualitatively and quantitatively similar to that of prostate as opposed to bladder [31].
• The present results demonstrate both inhibitory and stimulatory effects of glucocorticoid on androgen-induced proliferation of SC115 cells in cell culture and probably in vivo [21].
• An immunoblotting technique was used to study the forms of ornithine decarboxylase present in androgen-induced mouse kidney [32].
• Androgen-induced regeneration after castration was enhanced at day 3 by two-fold in mice expressing ectopic caFGFR1 [33].
• Whole-mount autoradiography study of DNA synthetic activity during postnatal development and androgen-induced regeneration in the mouse prostate [34].

References