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Nicotine Functions as Growth Factor to Fuel Tumor Proliferation: Study

NEW YORK (Reuters Health) Jul 31 - Scientists from the University of South Florida in Tampa say they have a new understanding of the molecular mechanisms underlying nicotine's ability to induce tumor cell proliferation and progression.

Their studies, reported online July 20th in the Journal of Clinical Investigation, suggest that nicotine functions like a growth factor and that the presence of nicotinic acetylcholine receptors (nAChRs) are key players in nicotine-induced cell proliferation. nAChRs bind nicotine and are present on bronchial cells as well as on lung cancer cells.

"While there is no evidence that nicotine contributes to the induction of tumors, it has been demonstrated that nicotine promotes the growth of solid tumors in vivo, suggesting that nicotine might be contributing to the progression of tumors already initiated," note Dr. Piyali Dasgupta and colleagues. But until now it has been unclear which molecules mediate these events.

Dr. Dasgupta's team showed that stimulation of non-small cell lung cancer (NSCLC) cells, as well as bronchial cells, with physiologic doses of nicotine leads to robust cell proliferation that is dependent on nAChRs.

The mitogenic effects of nicotine are "analogous to those of growth factors," the authors report, and involve recruitment of the scaffolding protein beta-arrestin to nicotine receptors, which facilitates activation of the tyrosine kinase Src, leading to the binding of the signaling kinase Raf-1 to the Rb protein.

The finding that levels of Rb-Raf1 complexes in human NSCLC tumors were greater than those in adjacent normal tissues "suggests that the Rb-Raf1 pathway probably contributes to oncogenesis," the team writes.

They also observed that disruption of the Rb-Raf1 interaction blocks nicotine-induced cell proliferation of NSCLC cells.

"Elucidation of the signaling events mediated by nAChRs present on non-neuronal cells," the authors conclude, "may open new avenues for targeting cancer therapy, focusing on agents that inhibit the beta-arrestin-Src signaling axis or Rb-Raf1 interaction."

Dr. Dasgupta's group also notes that "while tobacco carcinogens can initiate and promote tumorigenesis, the results of the present study raise the possibility that exposure to nicotine, by either cigarette substitutes or nicotine supplements, might confer a proliferative advantage to tumors already initiated."

This contention is supported by the findings that nicotine can protect NSCLC cells from apoptosis induced by chemotherapeutic agents. Moreover, it's been shown that smokers respond less well to chemotherapy and are at increased risk for metastasis.

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