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CorrigendumOncology Free access | 10.1172/JCI28164C1

Nicotine induces cell proliferation by β-arrestin–mediated activation of Src and Rb–Raf-1 pathways

Piyali Dasgupta, Shipra Rastogi, Smitha Pillai, Dalia Ordonez-Ercan, Mark Morris, Eric Haura, and Srikumar Chellappan

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Published November 1, 2006 - More info

Published in Volume 116, Issue 11 on November 1, 2006
J Clin Invest. 2006;116(11):3083–3083. https://doi.org/10.1172/JCI28164C1.
© 2006 The American Society for Clinical Investigation
Published November 1, 2006 - Version history
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Nicotine induces cell proliferation by β-arrestin–mediated activation of Src and Rb–Raf-1 pathways
Piyali Dasgupta, … , Eric Haura, Srikumar Chellappan
Piyali Dasgupta, … , Eric Haura, Srikumar Chellappan
Research Article Oncology

Nicotine induces cell proliferation by β-arrestin–mediated activation of Src and Rb–Raf-1 pathways

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Abstract

Recent studies have shown that nicotine, a component of cigarette smoke, can stimulate the proliferation of non-neuronal cells. While nicotine is not carcinogenic by itself, it has been shown to induce cell proliferation and angiogenesis. Here we find that mitogenic effects of nicotine in non–small cell lung cancers (NSCLCs) are analogous to those of growth factors and involve activation of Src, induction of Rb–Raf-1 interaction, and phosphorylation of Rb. Analysis of human NSCLC tumors show enhanced levels of Rb–Raf-1 complexes compared with adjacent normal tissue. The mitogenic effects of nicotine were mediated via the α7-nAChR subunit and resulted in enhanced recruitment of E2F1 and Raf-1 on proliferative promoters in NSCLC cell lines and human lung tumors. Nicotine stimulation of NSCLC cells caused dissociation of Rb from these promoters. Proliferative signaling via nicotinic acetylcholine receptors (nAChRs) required the scaffolding protein β-arrestin; ablation of β-arrestin or disruption of the Rb–Raf-1 interaction blocked nicotine-induced proliferation of NSCLCs. Additionally, suppression of β-arrestin also blocked activation of Src, suppressed levels of phosphorylated ERK, and abrogated Rb–Raf-1 binding in response to nicotine. It appears that nicotine induces cell proliferation by β-arrestin–mediated activation of the Src and Rb–Raf-1 pathways.

Authors

Piyali Dasgupta, Shipra Rastogi, Smitha Pillai, Dalia Ordonez-Ercan, Mark Morris, Eric Haura, Srikumar Chellappan

×

Original citation: J. Clin. Invest.116:2208-2217 (2006). doi:10.1172/JCI28164

Citation for this corrigendum: J. Clin. Invest.116:3083 (2006). doi:10.1172/JCI28164C1

During the preparation of this manuscript, an error was introduced in Figure 1A. The corrected Figure 1A appears below.

The authors regret this error.

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