Aromatase overexpression in dysfunctional adipose tissue links obesity to postmenopausal breast cancer

被引:90
|
作者
Wang, Xuyi [1 ,2 ]
Simpson, Evan R. [1 ,3 ]
Brown, Kristy A. [1 ,2 ]
机构
[1] Monash Univ, Metab & Canc Lab, Ctr Canc Res, Hudson Inst Med Res, Clayton, Vic, Australia
[2] Monash Univ, Dept Physiol, Clayton, Vic 3168, Australia
[3] Monash Univ, Dept Biochem & Mol Biol, Clayton, Vic, Australia
基金
澳大利亚国家健康与医学研究理事会;
关键词
Obesity; Aromatase; Breast cancer; Adipose; Stromal cells; NECROSIS-FACTOR-ALPHA; LIVER RECEPTOR HOMOLOG-1; ADJUVANT ENDOCRINE THERAPY; PROSTAGLANDIN E-2; STROMAL CELLS; INSULIN-RESISTANCE; PROMOTER-II; HORMONE CONCENTRATIONS; PI3K/AKT/MTOR PATHWAY; EPITHELIAL-CELLS;
D O I
10.1016/j.jsbmb.2015.07.008
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The number of breast cancer cases has increased in the last a few decades and this is believed to be associated with the increased prevalence of obesity worldwide. The risk of breast cancer increases with age beyond menopause and the relationship between obesity and the risk of breast cancer in postmenopausal women is well established. The majority of postmenopausal breast cancers are estrogen receptor (ER) positive and estrogens produced in the adipose tissue promotes tumor formation. Obesity results in the secretion of inflammatory factors that stimulate the expression of the aromatase enzyme, which converts androgens into estrogens in the adipose tissue. Evidence demonstrating a link between obesity and breast cancer has led to the investigation of metabolic pathways as novel regulators of estrogen production, including pathways that can be targeted to inhibit aromatase specifically within the breast. This review aims to present some of the key findings in this regard. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:35 / 44
页数:10
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