Nicotine-Mediated Cell Proliferation and Angiogenesis: New Twists to an Old Story

Piyali Dasgupta and Srikumar Chellappan

volume 5 | issue 20

15 october 2006
Pages: 2324 - 2328

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Tobacco smoking is one of the major etiologic factors associated with cancer. While there are many carcinogenic compounds present in tobacco smoke, its main addictive component, nicotine, is not carcinogenic by itself. The addictive properties of nicotine are achieved through the nicotinic acetylcholine receptors (nAChRs) that are widely distributed in the brain and neuromuscular junctions; at the same time, they were found to be expressed in a variety of non-neuronal tissues in the body including those of the lung. Recent studies show that these non-neuronal nAChRs can induce cell proliferation and angiogenesis. Analysis of the molecular mechanisms underlying nicotine-mediated cell proliferation showed the involvement of Src kinase and the scaffolding protein β-arrestin-1. Further, nAChRs were found to activate the basic components of the cell cycle machinery similar to growth factor receptors. This involved increased binding of Raf-1 kinase to the Rb protein, activation of cyclins D and E as well as induction of proliferative promoters. This article describes pathway involved in nicotine-induced cell proliferation and angiogenesis and the potential steps that are amenable for developing novel anti-cancer therapies.

Authors

Piyali Dasgupta

University of South Florida, Tampa, FL

Srikumar Chellappan

University of South Florida, H. Lee Moffit Cancer Center; Tampa, FL

We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link: