[HTML][HTML] Long-term exposure to nicotine, via ras pathway, induces cyclin D1 to stimulate G1 cell cycle transition
M Chu, J Guo, CY Chen - Journal of Biological Chemistry, 2005 - ASBMB
Nicotine, a major component in tobacco, has been implicated as a potential factor that
promotes the development of lung cancer. However, the molecular mechanism of its action
is still unclear. In this study, we have shown that, via nicotinic acetylcholine receptors,
persistent exposure of mouse epithelial cells to nicotine elicits Ras signaling and
subsequent Raf/MAP kinase activity, accompanied by a significant increase in cyclin D1
promoter activity and its protein expression. AP-1 is required for activation of the cyclin D1 …
promotes the development of lung cancer. However, the molecular mechanism of its action
is still unclear. In this study, we have shown that, via nicotinic acetylcholine receptors,
persistent exposure of mouse epithelial cells to nicotine elicits Ras signaling and
subsequent Raf/MAP kinase activity, accompanied by a significant increase in cyclin D1
promoter activity and its protein expression. AP-1 is required for activation of the cyclin D1 …