Department of Medicine, Weill Cornell Medicine, New York, USA; Graduate School of Medical Sciences, Weill Cornell Medicine, New York, USA.
Department of Medicine, Weill Cornell Medicine, New York, USA.
J Steroid Biochem Mol Biol. 2019 May;189:161-170. doi: 10.1016/j.jsbmb.2019.03.002. Epub 2019 Mar 6.
Obesity is a risk factor for estrogen receptor-positive (ER+) breast cancer after menopause. The pro-proliferative effects of estrogens are well characterized and there is a growing body of evidence to also suggest an important role in tumorigenesis. Importantly, obesity not only increases the risk of breast cancer, but it also increases the risk of recurrence and cancer-associated death. Aromatase is the rate-limiting enzyme in estrogen biosynthesis and its expression in breast adipose stromal cells is hypothesized to drive the growth of breast tumors and confer resistance to endocrine therapy in obese postmenopausal women. The molecular regulation of aromatase has been characterized in response to many obesity-related molecules, including inflammatory mediators and adipokines. This review is aimed at providing an overview of our current knowledge in relation to the regulation of estrogens in adipose tissue and their role in driving breast tumor development, growth and progression.
肥胖是绝经后雌激素受体阳性(ER+)乳腺癌的一个危险因素。雌激素的促增殖作用已得到充分证实,越来越多的证据表明其在肿瘤发生中也起着重要作用。重要的是,肥胖不仅会增加乳腺癌的风险,还会增加复发和与癌症相关的死亡风险。芳香化酶是雌激素生物合成的限速酶,其在乳腺脂肪基质细胞中的表达被假设为驱动乳腺肿瘤的生长,并使肥胖绝经后妇女对内分泌治疗产生耐药性。芳香化酶的分子调节已经针对许多与肥胖相关的分子进行了描述,包括炎症介质和脂肪因子。这篇综述旨在概述我们目前在脂肪组织中雌激素的调节及其在驱动乳腺肿瘤发生、生长和进展中的作用方面的知识。