A role for FGF2 in visceral adiposity-associated mammary epithelial transformation
A role for FGF2 in visceral adiposity-associated mammary epithelial transformation
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DOI：
10.1080/21623945.2018.1445889
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发表时间：
2018-01-01
期刊：
影响因子：
3.3
通讯作者：
Bernard, Jamie J.
中科院分区：
文献类型：
--
作者：
Benham, Vanessa;Chakraborty, Debrup;Bernard, Jamie J.
肥胖是绝经后乳腺癌的主要风险因素，这一点令人担忧，因为2014年40%的癌症诊断与超重/肥胖有关。尽管存在这种流行病学联系，但其潜在的致病机制尚不清楚。我们最近发表了内脏脂肪组织(VAT)释放FGF2并刺激皮肤上皮细胞转化的研究报告。此外，肥胖与许多上皮性癌症有不同的关联，这种机制上的联系可能是转译的。由于FGF2和FGFR1与乳腺癌的进展有关，我们推测增值税衍生的FGF2在促进肥胖相关的乳腺上皮细胞转化中起着翻译作用。在这份简短的报告中，数据表明FGF2/FGFR1信号是增值税刺激的乳腺上皮细胞转化的潜在机制联系。
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.