Cellular and molecular mechanisms of nicotine's pro-angiogenesis activity and its potential impact on cancer

被引：51

作者：

Mousa, S ^{[1
]}

Mousa, SA ^{[1
]}

机构：

[1] Albany Coll Pharm, Pharmaceut Res Inst, Albany, NY 12208 USA

来源：

JOURNAL OF CELLULAR BIOCHEMISTRY | 2006年 / 97卷 / 06期

关键词：

angiogenesis; dermal fibroblast; endothelial cell; fibroblast growth factor; nicotine; tumor growth;

D O I：

10.1002/jcb.20741

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 present study examined the mechanisms of nicotine's effect on angiogenesis and its impact on tumor growth. Nicotine demonstrated significant (P < 0.01) stimulation of the release of endothelial cell growth factor, basic fibroblast growth factor (b-FGF) but not vascular endothelial growth factor (VEGF). In a concentration-dependent manner, nicotine induced endothelial cell tube formation. Additionally, in the chick chorioallantoic membrane (CAM) model of angiogenesis, nicotine effectively induced the generation of new blood vessels (P < 0.01), an effect that is mediated via b-FGF. The pro-angiogenesis effect of nicotine in the CAM model was maximally blocked by either anti-integrin alpha(v)beta(3) or inhibitor of mitogen activated protein kinase (MAPK, ERK 1/2). In the CAM tumor implant model, nicotine doubled (P < 0.01) the growth rate of breast, colon, and lung cancer. These data indicated that the pro-angiogenesis effect is mediated via b-FGF and induced through the nicotinic receptor, alpha(v)beta(3) integrin, and MAPK.

引用

页码：1370 / 1378

页数：9

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