Author of

• 13580

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  P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)

  • Event: WCLC 2015
  • Type: Poster
  • Track: Biology, Pathology, and Molecular Testing
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)

  • 13696

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    P1.04-116 - The Role of JAK/STAT3 Signaling Pathway on Apoptosis of Lung Adenocarcinoma Cell Line PC-9 Induced by Icotinib (ID 2263)

    09:30 - 09:30  |  Author(s): Z. Niu
    • Abstract

    Background:
    The aim of the study is to estimate the role of JAK/STAT3 signaling pathway on apoptosis of lung adenocarcinoma induced by icotinib.
    
    Methods:
    EGFR mutation was detected in lung adenocarcinoma cell line PC-9 by ARMS assay; The inhibitory rates of cell proliferation, at different concentrations (0 ~ 100 umol/L) of icofinib and continued incubating for 24，48 and 72 h respectively, were evaluated by MTT assay; Apoptosis of PC-9 cells exposured to different concentrations of icotinib(0, 0.1, 1 and 10 umol/L) for 48 h were evaluated by TUNEL assay; JAK2, STAT3, Bcl-2, Bax mRNA expressions were evaluated by Real-time PCR assay; The protein levels of P-STAT3 and IL-6 were evaluated by Western-blot assay.
    
    Results:
    Human lung adenocarcinoma cell line PC-9 had an exon 19 deletion mutation in EGFR gene; Followed by treatment of icotinib，the proliferation of PC-9 cells were all inhibited significantly, especially in 48 and 72 h (P<0.01) in all concentrations; The inhibitory rates of cell proliferation in different treating time had statistical significance (P<0.01); Cell apoptosis at different concentrations were increased significantly (P<0.05); Along with the increasing concentrations, gen expression levels of JAK2, STAT3 and Bcl-2 decreased significantly (P<0.05), Bax increased significantly (P<0.05), JAK2/STAT3 ratios increased significantly (P<0.01), and Bcl-2/bax ratios decreased significantly (P<0.01); P-STAT3 and IL-6 protein levels were inhibited significantly at by higher concentration.
    
    Conclusion:
    JAK/STAT3 signaling pathway take a participate in apoptosis of PC-9 cells induced by icotinib. The most likely mechanism is icotinib inhibited the gen expression levels of JAK2, STAT3 and Bcl-2, so with the P-STAT3 and IL-6 protein levels, and mediated gene Bax overexpression.