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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Caveolin-1 down-regulation activates estrogen receptor alpha expression and leads to 17beta-estradiol-stimulated mammary tumorigenesis.
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Caveolin-1 down-regulation activates estrogen receptor alpha expression and leads to 17beta-estradiol-stimulated mammary tumorigenesis.

机译：Caveolin-1下调激活雌激素受体α表达，并导致17β-雌二醇刺激的乳腺肿瘤发生。

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摘要

Constitutive activation of estrogen receptor alpha (ER-alpha) expression is an early event in breast cancer tumorigenesis. However, the mechanism whereby ER-alpha is constitutively activated during transformation of normal mammary cells has not been well established. Previously, we reported that haploinsufficiency of caveolin-1, a major structural protein that forms caveolae, resulted in anchorage-independent growth of a normal mammary epithelial cell line, MCF10A. Here, we further demonstrated that ER-alpha but not ER-beta expression was constitutively activated in these caveolin-1 haploinsufficient cells. Transient treatment of MCF10A cells with beta-methyl-cyclodextrin, a chemical that can displace caveolin-1 from the plasma membrane, also stimulated ER-alpha expression. We further found that the 17beta-estradiol (E2) accelerated anchorage-independent growth of these cells in vitro and promoted their tumorigenesis in nude mice. These results suggest that dysregulation of caveolin-1 is one of the mechanisms by which ER-alpha expression is activated during initiation of breast tumorigenesis.
机译：雌激素受体α（ER-α）表达的组成性激活是乳腺癌肿瘤发生中的早期事件。然而，在正常乳腺细胞转化过程中ER-α被组成性激活的机制尚未完全建立。以前，我们报道了小窝蛋白1的单倍不足，形成小窝的一种主要结构蛋白，导致正常乳腺上皮细胞系MCF10A的锚定非依赖性生长。在这里，我们进一步证明，在这些caveolin-1单倍体不足的细胞中，ER-α表达而非ER-β表达被组成性激活。用β-甲基-环糊精短暂处理MCF10A细胞（一种可以从质膜上置换小窝蛋白1的化学物质）也刺激了ER-α的表达。我们进一步发现17β-雌二醇（E2）在体外加速了这些细胞的锚定非依赖性生长，并促进了它们在裸鼠中的肿瘤发生。这些结果表明，caveolin-1的失调是在乳腺肿瘤发生过程中激活ER-α表达的机制之一。

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