Author of

• 25923

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  P1.03 - Biology (Not CME Accredited Session) (ID 935)

  • Event: WCLC 2018
  • Type: Poster Viewing in the Exhibit Hall
  • Track:
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/24/2018, 16:45 - 18:00, Exhibit Hall

  • 26418

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    P1.03-21 - Huaier Aqueous Extract Induces Lung Adenocarcinoma Cell Apoptosis Through Excessive Activation Of MEK/ERK Signaling Pathway (ID 12019)

    16:45 - 18:00  |  Author(s): Chundong Gu
    • Abstract
    • Slides

    Background
    

    As the most important pathological types of lung cancer, adenocarcinoma has poor prognosis due to the characteristics of early metastasis and recurrence even in effective surgery, radiotherapy and chemotherapy. In China, Traditional Chinese medicine “Huaier aqueous extract” (HAE) is widely used in antineoplastic treatment, but its molecular mechanism in lung adenocarcinoma remains unclear. This study aimed to explore the apoptotic mechanism of HAE in lung adenocarcinoma.

    a9ded1e5ce5d75814730bb4caaf49419 Method
    

    MTT assay and flow-cytometric analysis were measured to identify the cell viability and apoptosis rate affected by HAE in human lung adenocarcinoma A549, H322 cell. Immunofluorescence assay was applied to examine the effect of HAE on expression and distribution of Cytochrome C and ERK1/2 in A549, H322 cell. Further, A549 cell was respectively treated with HAE and subjected to western blotting for protein level of MEK/ERK signaling pathway. In human trials, a total of 40 patients with stage I lung adenocarcinoma after complete resection were enrolled from January 2015 to December 2016. 20 of them were given HAE and others were not, and then the patients’ 3-year disease free survival was examined.

    4c3880bb027f159e801041b1021e88e8 Result
    

    HAE significantly inhibited the cell viability of A549, H322 cell in dose-dependent and time--dependent manner. Further, HAE induced accumulation of Cytochrome C, an apoptosis core factor, in cytoplasm and promote the apoptosis of A549, H322 cells. Meanwhile, HAE launched the expression of ERK1/2 and the latter migrated more to the nucleus following with excessive activation of MEK/ERK signaling pathway. The patients treated with HAE showed fewer recurrences than the rest (3-year disease free survival: 93.8% vs 71.4%; P=0.048).

    8eea62084ca7e541d918e823422bd82e Conclusion
    

    HAE could over-activate MEK/ERK signaling pathway and exert apoptosis-inducing effects in lung adenocarcinoma.

    6f8b794f3246b0c1e1780bb4d4d5dc53

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• 25940

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  P2.03 - Biology (Not CME Accredited Session) (ID 952)

  • Event: WCLC 2018
  • Type: Poster Viewing in the Exhibit Hall
  • Track:
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/25/2018, 16:45 - 18:00, Exhibit Hall

  • 26960

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    P2.03-23 - MicroRNA-30e Inhibits Cell Proliferation and Invasion in Non-Small Cell Lung Cancer via Directly Targeting SOX9 (ID 12848)

    16:45 - 18:00  |  Author(s): Chundong Gu
    • Abstract
    • Slides

    Background
    

    Previous studies reported that microRNA-30e (miR-30e) was dysregulation in multiple human cancers. However, the expression, functions and molecular mechanism of miR-30e in NSCLC remains unknown. In this study, we found that miR-30e expressed at low levels in NSCLC tissues and NSCLC cell lines.

    a9ded1e5ce5d75814730bb4caaf49419 Method
    

    The miR-30e expression was texted in NSCLC tissues and cell lines by RT-qPCR. We then overexpressed miR-30e expression in NSCLC cells to evaluate its effects in regulating NSCLC proliferation and invasion in vitro. Moreover, the mechanisms underlying the biological roles of miR-30e in NSCLC were investigated using luciferase reporter assay.

    4c3880bb027f159e801041b1021e88e8 Result
    

    In NSCLC cell lines, enforced expression of miR-30e inhibited cell proliferation and invasion in vitro. In addition, miR-30e negatively regulated SOX9 expression through directly binding to the 3'UTR of SOX9, and an inverse correlation was found between miR-30e and SOX9 mRNA expression level in NSCLC tissues. Moreover, SOX9 knockdown led to decreased proliferation and invasion of NSCLC cells.

    8eea62084ca7e541d918e823422bd82e Conclusion
    

    miR-30e is downregulated in NSCLC and inhibits cell proliferation and invasion, possibly by directly targeting SOX9.

    6f8b794f3246b0c1e1780bb4d4d5dc53

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