DHT and testosterone, but not DHEA or E2, differentially modulate IGF-I, IGFBP-2, and IGFBP-3 in human prostatic stromal cells.

作者: Hanh Le , Julia T. Arnold , Kimberly K. McFann , Marc R. Blackman

DOI: 10.1152/AJPENDO.00451.2005

关键词: Internal medicineEndocrinologyDehydroepiandrosteroneAndrogen receptorDihydrotestosteroneStromal cellProstate cancerTestosteroneFlutamideAndrogenBiology

摘要: Prostate cancer is one of the four most common cancers in United States, affecting six men. Increased serum levels androgens and IGF-I are associated with an augmented risk prostate cancer. Dihydrotestosterone (DHT) testosterone (T) stimulate cell growth, development, function, whereas effects DHT T stromal cells, dehydroepiandrosterone (DHEA) or uncertain. We investigated actions DHT, T, DHEA, estradiol (E2) on insulin-like growth factor (IGF)-I, IGF-II, receptor (R), IGF-binding protein (IGFBP)-2, IGFBP-3, IGFBP-5 primary cultures human prostatic cells by assessing proliferation, mRNA expression, secretion MTT assay, quantitative real-time PCR, ELISA, respectively. each increased (7-fold) decreased IGFBP-3 (2-fold) expression a dose- time-dependent manner IGFBP-2 manner. DHEA E2 did not significantly alter these measures. Flutamide abolished DHT-modulated increases IGFBP-2, suggesting that influences measures were androgen mediated. None steroids affected IGF-IR, proliferation. The IGF-I, more pronounced express desmin. These data suggest promote partly via modulation IGF axis, potential paracrine epithelial cells.

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