A role for FGF2 in visceral adiposity-associated mammary epithelial transformation

被引：15
作者：
Benham, Vanessa [1 ]
Chakraborty, Debrup [1 ]
Bullard, Blair [1 ]
Bernard, Jamie J. [1 ]
机构：
[1] Michigan State Univ, Dept Pharmacol & Toxicol, E Lansing, MI 48824 USA
来源：
ADIPOCYTE | 2018年 / 7卷 / 02期
关键词：
Obesity; cancer; FGF2; adiposity; visceral fat; breast; breast cancer; BREAST-CANCER RISK; GROWTH-FACTOR RECEPTOR; BODY-MASS INDEX; WAIST CIRCUMFERENCE; THERAPEUTIC TARGET; OBESITY PHENOTYPES; FACTOR FAMILY; CELLS; TISSUE; PROLIFERATION;
D O I：
10.1080/21623945.2018.1445889
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Obesity is a leading risk factor for post-menopausal breast cancer, and this is concerning as 40% of cancer diagnoses in 2014 were associated with overweight/obesity. Despite this epidemiological link, the underlying mechanism responsible is unknown. We recently published that visceral adipose tissue (VAT) releases FGF2 and stimulates the transformation of skin epithelial cells. Furthermore, obesity is differentially associated with many epithelial cancers, and this mechanistic link could be translational. As FGF2 and FGFR1 are implicated in breast cancer progression, we hypothesize that VAT-derived FGF2 plays a translational role in promoting adiposity-associated mammary epithelial cell transformation. In this brief report, data suggest that FGF2/FGFR1 signaling is a potential mechanistic link in VAT-stimulated transformation of breast epithelial cells.
引用
收藏
页码：113 / 120
页数：8
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