Cellular and molecular mechanisms of nicotine's pro-angiogenesis activity and its potential impact on cancer
✍ Scribed by Sarah Mousa; Shaker A. Mousa
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 253 KB
- Volume
- 97
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
Abstract
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 α~v~β~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, α~v~β~3~ integrin, and MAPK. J. Cell. Biochem. 97: 1370–1378, 2006. © 2005 Wiley‐Liss, Inc.