Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Division of Reproductive Science in Medicine, Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Robert H. Lurie Comprehensive Cancer Center, 303 E. Superior Street, Suite 4-121, Chicago, IL, 60611, USA.
Horm Cancer. 2018 Aug;9(4):229-239. doi: 10.1007/s12672-018-0329-6. Epub 2018 Mar 15.
Obesity is associated with increased risk of breast cancer in postmenopausal but not in premenopausal women. Many factors may be responsible for this difference. The aim of this study was to determine the mechanisms by which the genes related to the AMPK pathway, inflammation, and estrogen actions are affected by adiposity in breast tissue with the objective of identifying differences that may explain the different breast cancer risk in premenopausal and postmenopausal women. Random fine needle aspirates (rFNAs) of breast tissue were collected from 57 premenopausal and 55 postmenopausal women and were classified as normal weight, overweight, or obese. Expression levels of 21 target genes were determined using a TaqMan Low Density Array procedure. Breast tissue estradiol levels were measured by a liquid chromatography-tandem mass spectrometry procedure, and serum estradiol and follicle-stimulating hormone (FSH) were measured by a radioimmunoassay and an enzyme-linked immunosorbent assay, respectively. We found that in postmenopausal women, serum and tissue estradiol levels were increased in those who were overweight, and serum FSH levels were decreased in obese status. Interestingly, RPS6KB1, an AMPK downstream-responsive gene for protein synthesis and cell growth, and estrogen receptor α (encoded by the ESR1 gene) and its target gene GATA3 were significantly decreased in rFNA of premenopausal, obese women. In postmenopausal women, RPS6KB1, ESR1, and GATA3 expression remained unchanged in relation to adiposity. However, prostaglandin-endoperoxide synthase 2 (PTGS2), cyclin D1 (CCND1), and another ESR1 target gene, TFF1, were elevated in rFNA of obese postmenopausal women. Thus, as bodyweight increases, gene expression is indicative of increased proliferation in postmenopausal women but decreased proliferation in premenopausal women. Overall, our data reveal a novel process by which obesity promotes the risk of breast cancer in postmenopausal but not premenopausal women.
肥胖与绝经后妇女乳腺癌风险增加相关,但与绝经前妇女无关。许多因素可能导致这种差异。本研究旨在确定与 AMPK 通路、炎症和雌激素作用相关的基因在乳腺组织中受肥胖影响的机制,目的是确定可能解释绝经前和绝经后妇女乳腺癌风险不同的差异。从 57 名绝经前和 55 名绝经后妇女中随机采集细针穿刺乳腺组织 (rFNA),并将其分为正常体重、超重或肥胖。使用 TaqMan 低密度阵列程序测定 21 个靶基因的表达水平。采用液相色谱-串联质谱程序测定乳腺组织雌二醇水平,采用放射免疫法和酶联免疫吸附法分别测定血清雌二醇和卵泡刺激素 (FSH)。我们发现,在绝经后妇女中,超重者血清和组织雌二醇水平升高,肥胖者血清 FSH 水平降低。有趣的是,RPS6KB1 是 AMPK 下游参与蛋白合成和细胞生长的基因,以及雌激素受体 α (ESR1 基因编码) 和其靶基因 GATA3 在绝经前肥胖妇女的 rFNA 中显著降低。在绝经后妇女中,RPS6KB1、ESR1 和 GATA3 的表达与肥胖无关。然而,前列腺素内过氧化物合酶 2 (PTGS2)、周期蛋白 D1 (CCND1) 和另一个 ESR1 靶基因 TFF1 在肥胖绝经后妇女的 rFNA 中升高。因此,随着体重增加,基因表达表明绝经后妇女的增殖增加,但绝经前妇女的增殖减少。总的来说,我们的数据揭示了一种新的机制,即肥胖增加了绝经后妇女乳腺癌的风险,但不会增加绝经前妇女的乳腺癌风险。