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  P3.01 - Poster Session with Presenters Present (ID 469)

  • Event: WCLC 2016
  • Type: Poster Presenters Present
  • Track: Biology/Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)

  • 18307

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    P3.01-035 - Nicotine Enhances Hepatocyte Growth Factor-Mediated Lung Cancer Cell Migration (ID 3860)

    14:30 - 14:30  |  Author(s): R. Yoneyama
    • Abstract
    • Slides

    Background:
    Cigarette smoking not only promotes lung carci­nogenesis, but it has also been demonstrated to promote the progression of lung cancer. Despite nicotine being a major component of cigarette smoke, it is not carcinogenic when acting alone. Instead, it is believed to function as a tumor promoter that stimulates the processes of invasion and metastasis. In the present study we aimed to determine the effect of nicotine on the migratory activity of lung cancer cells.
    
    Methods:
    The effect of nicotine on the migration of lung cancer A549 cells was evaluated by a wound healing assay. Hepatocyte growth factor (HGF) was used as a pro‑migratory stimulus. During several of the experiments, specific inhibitors of α7‑nicotine acetylcholine receptor (α7‑nAchR), phosphoinositide kinase‑3 (PI3K) and extracellular signal‑related kinase (ERK)1/2 were included. The phosphorylation levels of Akt and ERK1/2 were examined using a cell‑based protein phosphorylation assay.
    
    Results:
    Nicotine did not induce cell migration by itself, but it instead promoted HGF‑induced cell migra­tion (Figure). The effects of nicotine were inhibited by the pretreatment of the cells with the α7‑nAchR inhibitor, methyllycaconitine, and the PI3K inhibitor, LY294002. The mitogen‑activated protein kinase/ERK kinase kinase inhibitor exerted modest, but non‑significant inhibitory activity on the effect of nicotine. Nicotine did not induce Akt phosphorylation by itself, but instead promoted the HGF‑induced phosphorylation of Akt. It was also observed that nicotine had no effect on ERK1/2 phosphorylation.Figure 1
    
    
    
    Conclusion:
    These results indicate that nicotine, when alone, does not have a pro‑migratory func­tion, but instead enhances responsiveness to the pro‑migratory stimulus emitted by HGF. This study provides an insight into the mechanism of tumor promotion by demonstrating that nicotine and α7‑nAchRs act in synergy with the HGF‑induced PI3K/Akt signaling pathway, increasing the sensitivity of lung cancer cells to HGF, and thereby promoting cell migration, a vital step in invasion and metastasis.
    
    

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