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高脂饮食诱导的大鼠乳腺癌模型

High Fat Diet-induced Breast Cancer Model in Rat.

作者信息

Wu Meng-Ju, Chang Chun-Ju

机构信息

Department of Basic Medical Sciences, Purdue University, West Lafayette, Indiana, USA.

Center for Cancer Research, Purdue University, West Lafayette, Indiana, USA.

出版信息

Bio Protoc. 2016 Jul 5;6(13). doi: 10.21769/BioProtoc.1852.

DOI:10.21769/BioProtoc.1852
PMID:28573159
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5448410/
Abstract

Obesity has been linked to breast cancer progression but the underlying mechanisms remain obscure. Being overweight or obese for a woman at the time she is diagnosed with breast cancer is linked to a high risk of recurrence regardless of treatment factors. In rodents, high body weight is also associated with increased incidence of spontaneous and chemically induced tumors. To study the complex interaction between the mammary epithelia and the microenvironment, with a focus on the mechanism underlying the role obesity plays in the regulation of the cancer stem cell traits and the development of mammary cancer , we have established a diet-induced obesity (DIO) rat model of breast cancer (Chang ., 2015).

摘要

肥胖与乳腺癌进展有关,但其潜在机制仍不清楚。女性在被诊断患有乳腺癌时超重或肥胖与复发风险高有关,而与治疗因素无关。在啮齿动物中,高体重也与自发性和化学诱导性肿瘤的发病率增加有关。为了研究乳腺上皮细胞与微环境之间的复杂相互作用,重点关注肥胖在调节癌症干细胞特性和乳腺癌发展中所起作用的潜在机制,我们建立了饮食诱导肥胖(DIO)大鼠乳腺癌模型(Chang等,2015年)。

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High Fat Diet-induced Breast Cancer Model in Rat.高脂饮食诱导的大鼠乳腺癌模型
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Obesity, independent of p53 gene dosage, promotes mammary tumor progression and upregulates the p53 regulator microRNA-504.肥胖症(与 p53 基因剂量无关)可促进乳腺肿瘤的发展,并上调 p53 调节 microRNA-504。
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Obesity reversibly depletes the basal cell population and enhances mammary epithelial cell estrogen receptor alpha expression and progenitor activity.肥胖症可使基底细胞群体减少,并增强乳腺上皮细胞雌激素受体α的表达和祖细胞活性。
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本文引用的文献

1
Leptin-STAT3-G9a Signaling Promotes Obesity-Mediated Breast Cancer Progression.瘦素-信号转导和转录激活因子3-组蛋白甲基转移酶G9a信号通路促进肥胖介导的乳腺癌进展。
Cancer Res. 2015 Jun 1;75(11):2375-2386. doi: 10.1158/0008-5472.CAN-14-3076. Epub 2015 Apr 3.
2
Humane endpoints and cancer research.人道终点与癌症研究。
ILAR J. 2000;41(2):87-93. doi: 10.1093/ilar.41.2.87.