Induction by estrogen metabolite 16 alpha-hydroxyestrone of genotoxic damage and aberrant proliferation in mouse mammary epithelial cells.
Induction by estrogen metabolite 16 alpha-hydroxyestrone of genotoxic damage and aberrant proliferation in mouse mammary epithelial cells.
复制标题
雌激素代谢物 16 α-羟基雌酮诱导小鼠乳腺上皮细胞的基因毒性损伤和异常增殖。
DOI：
10.1093/jnci/84.8.634
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Bradlow,HL
中科院分区：
文献类型：
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作者：
Telang,NT;Suto,A;Wong,GY;Osborne,MP;Bradlow,HL
背景：雌激素是有效的乳腺肿瘤促进剂，通过表观遗传机制影响启动后事件。上调（即，17β-雌二醇（E2）生物转化过程中C16α-羟基化途径的诱导作用与乳腺细胞转化有关。目的：本研究以C57 BL小鼠乳腺上皮细胞系C57/MG为研究对象，探讨E2及其代谢产物16-羟基雌酮（16-hydroxyestrone，16-hydroxyestrone（16α-OHE 1）和雌三醇（E3）作为乳腺细胞转化的起始剂发挥作用。DNA修复（对羟基脲不敏感的胸苷摄取）、雌激素代谢（3 H交换形成3 H20）、过度增殖（细胞数量增加）和获得锚定非依赖性细胞因子。
Background: Estrogens are potent mammary tumor promoters influencing post-initiational events via epigenetic mechanisms. The upregulation (i.e., induction) of the C16α-hydroxylation pathway during 17β-estradiol (E2) biotransformation has been associated with mammary cell transformation. The action of E2metabolites on tumorigenic transformation, however, is poorly understood.Purpose: The newly established mammary epithelial cell line C57/MG, derived from the C57BL mouse strain, was used to examine whether E2or its metabolites, 16-hydroxyestrone (16α-OHE1) and estriol (E3), function as initiators of mammary cell transformation.Methods: DNA repair (hydroxyurea-insensitive thymidine uptake), estrogen metabolism (3H exchange to form3H20), hyperproliferation (increased cell number), and acquisition of anchorage-independent