乳腺脂肪组织中芳香酶与乳腺癌的关系的研究进展  

Aromatase in adipose tissue: Relationship to breast cancer

作　　者：于正洪[1] 姜恩泽[2] 上官俊杰[3] 陈龙邦[1] 

机构地区：[1]南京军区南京总医院肿瘤内科,南京医学博士210002 [2]南京大学医学院,南京210008 [3]美国西北大学文理学院,芝加哥60611

出　　处：《医学研究生学报》2013年第12期1320-1325,共6页Journal of Medical Postgraduates

基　　金：国家自然科学基金(81272260);江苏省六大人才高峰基金(BK2009284)

摘　　要：肥胖可导致乳腺中芳香酶异常的高表达,增加局部雌激素的产生,造成乳腺增生和癌变的倾向。绝经女性的脂肪增加可触发一些能增加芳香酶表达的信号通路。在乳腺脂肪成纤维细胞中,局部前列腺素E2(prostaglandin E2,PGE2)产量的增加可能会诱导近端启动子区域,而肿瘤坏死因子(tumor necrosis factor,TNF)产量的升高可能会诱导芳香酶远端启动子。文章对控制芳香酶基因在乳腺脂肪组织中表达的机制,以及恶性乳腺上皮细胞和周围脂肪成纤维细胞的相互作用作一综述。对于这些信号通路的系统性描述将有利于发现特定的药物靶向目标,以便选择性地降低芳香酶的过表达,减少过多的雌激素产生,达到较好的疗效。It has been proved that obesity can lead to abnormally high expression of aromatase in the breast, higher local estrogen production, and possibility to breast cancer and hyperplasia. In postmenopausal women, increased adiposity may active signaling pathways that lead to a higher aromatase expression. A higher local prostaglandin E2 （PGE2） level in breast adipose fibroblasts may induce the proximal promoter region, and increased tumor necrosis factor （TNF） production in breast adipose fibroblasts may induce the distal promoters of aromatase. We review the mechanisms which control aromatase expression in breast adipose tissue, and the interactions between malignant breast epithelial cells and the surrounding adipose fibroblasts. These signaling pathways＇ systematic characterization will help the identification of potential drug targets to selectively reduce aromatase expression and excessive estrogen production, with therapeutic benefit.

关 键 词：乳腺癌 芳香酶 肥胖 

分 类 号：R737.9[医药卫生—肿瘤]