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Yu-Feng Wei

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    P3.03 - Biology (Not CME Accredited Session) (ID 969)

    • Event: WCLC 2018
    • Type: Poster Viewing in the Exhibit Hall
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 9/26/2018, 12:00 - 13:30, Exhibit Hall
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      P3.03-17 - Roles of α7nAchR Signaling in Lung Cancer (ID 13886)

      12:00 - 13:30  |  Presenting Author(s): Yu-Feng Wei

      • Abstract
      • Slides


      Lung cancer is the leading cause of cancer-related mortality worldwide. Cigarette smoking is the leading risk factor driving lung cancer. Nicotine, as the major addictive component in cigarettes, can stimulate the progression of lung cancer cells through nicotinic acetylcholine receptors (nAChRs). The nAChR α7 subunit has been found to be pivotal in growth signal transduction induced by nicotine binding to nAChRs in lung cancer cells. Nevertheless, its clinical roles remain unclear.

      a9ded1e5ce5d75814730bb4caaf49419 Method

      We firstly used the bioinformatics platform to analyze whether the messenger RNA (mRNA) expression of various nAChRs might contribute to patient survival. The immunohistochemistry was additionally applied to analyze the distribution patterns of α7nAchR protein in lung cancer. Complementary DNA (cDNA) microarray, immunoblotting analysis, and Cell Proliferation Kit II (XTT) assay were used to explore the potential effects and mechanisms.

      4c3880bb027f159e801041b1021e88e8 Result

      We found that patient groups with high CHRNA7 mRNA levels had an improved overall survival rate in 1926 lung cancer cases (p<0.001). Furthermore, increased CHRNA7 mRNA expression improved overall survival of squamous cell, but not adenocarcinoma, lung cancer patients (p=0.043). In addition, high CHRNA7 mRNA expression predicted better overall survival only in female patient group (P=0.001). Nuclear and cytoplasmic α7nAChR staining were significantly increased in cancerous and metastatic lesions as compared with adjacent non-cancerous tissues. Membranous α7nAChR staining was present only in cancerous lesions and was low in metastatic lesions. Notably, H157N cells have been harvested with nicotine for 2 years and had an increased α7nAChR expression. In addition, nicotine was able to increase α7nAChR expression in both H157 and H157N cells. Anti-α7nAChR antibody suppressed cell grow in only H157N cells despite of nicotine treatment with or without. Long term nicotine exposure might change the dependence of α7nAChR signaling in squamous lung cancer cells.

      8eea62084ca7e541d918e823422bd82e Conclusion

      Our results suggested that α7nAChR might play roles in squamous lung cancer and in female lung cancer. mRNA and protein levels of α7nAChR appear to represent a tumor suppressive or an oncogenic role, respectively. The exact roles and underlying mechanisms of the α7nAChR related signaling demand further investigations in particular squamous lung cancer patients with smoking history.


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