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CYP19A1 — IGF2

Text-mined interactions from Literome

Ferrari et al., Int J Oncol 1997 : Effects of aromatase complex selective inhibition on insulin-like growth factor 1 and insulin-like growth factor binding protein 3 circulating levels in breast cancer
Nestler et al., Endocrinology 1990 : Because pregnant diabetic women are reported to have lower serum estrogen and higher progesterone levels than nondiabetic pregnant women, and placental insulin-like growth factor II (IGF-II) production may be elevated during diabetic pregnancy, the role of IGF-II in the regulation of human cytotrophoblastic aromatase , 3 beta-hydroxysteroid dehydrogenase ( 3 beta HSD ), and P450 cholesterol side-chain cleavage ( P450scc ) enzyme activities was studied ... IGF-II could suppress aromatase activity at a concentration as low as 2.0 ng/ml. Preincubation of cells with either insulin, IGF-I, or a monoclonal anti-IGF-I receptor antibody did not alter IGF-II 's potent inhibitory effect ... These observations suggest that IGF-II suppresses aromatase activity by activation of its own specific receptor
Rigaudière et al., Acta Endocrinol (Copenh) 1989 : When related to time ( 0-4 h ) and expressed as percent of control values, aromatase activity in the presence of insulin, IGF-I and/or hCG exhibited a significant and transient increase at 15-30 min
Secreto et al., Anticancer Res 1994 (Breast Neoplasms...) : The elevated testosterone levels and the increased levels of insulin, IGF-I, and IGF-II that are seen in PCOS and abdominal obesity could favor the development of breast cancer in several ways, all of which have been demonstrated experimentally : binding of testosterone to cancer cells bearing testosterone receptors, with direct stimulation ; intratissular aromatization of testosterone to estradiol, with stimulation of estrogen-sensitive cells ; stimulation of the production of epithelial growth factor (EGF) by testosterone, with direct mitogenic effect of EGF on cancer cells ; stimulation of aromatase by insulin and IGF-I ; direct mitogenic stimulation of cancer cells by insulin, IGF-I, and IGF-II ; and stimulation by IGF-I and IGF-II of the intratissular reduction of estrone to estradiol
Giudice et al., Prog Growth Factor Res 1995 (Polycystic Ovary Syndrome) : It has been postulated that an inhibitor of IGF 's synergistic actions with FSH on aromatase activity may be one ( or more ) of the IGFBPs, which contributes to the arrested state of follicular development commonly observed in this disorder