Author of

• 16879

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  P1.07 - Poster Session with Presenters Present (ID 459)

  • Event: WCLC 2016
  • Type: Poster Presenters Present
  • Track: SCLC/Neuroendocrine Tumors
  • Presentations: 1
  • Moderators:
  • Coordinates: 12/05/2016, 14:30 - 15:45, Hall B (Poster Area)

  • 16904

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    P1.07-025 - MiR-495 Promotes Chemoresistance of SCLC through Epithelial-Mesenchymal Transition via Etk/BMX (ID 4077)

    14:30 - 14:30  |  Author(s): S. Fang
    • Abstract
    • Slides

    Background:
    MiR-495 is firstly found in the brain tissues and it can regulate neuronal plasticity by affecting the expression of brain-derived neurotropic factor. Studies have shown that the function of miR-495 is still controversial in different types of cancer. For example, it serves as a tumor suppressor in MLL-rearranged leukemia, while functions as an oncogenic miRNA in breast cancer. However, whether the miR-495 serves as a tumor suppressor or an oncogene in SCLC has not been reported.
    
    Methods:
    In this study, we investigated whether miR-495 regulates chemoresistance of SCLC through epithelial-mesenchymal transition (EMT) via Epithelial and endothelial tyrosine kinase (Etk/BMX) using two drug resistant cell lines. The expression of miR-495 and Etk/BMX in SCLC patients were examined in 86 SCLC tissues and 60 normal lung tissues by qRT-PCR and Immunohistochemical staining.
    
    Results:
    Loss- and gain-of-function experiments showed miR-495 regulated cells proliferation, tumor growth and drug resistance. MiR-495 suppression or Etk/BMX elevation in SCLC specimens correlated with poor pathologic stage and survival time. The expression of Etk/BMX was one of the directly targeted genes of miR-495. Ectopic expression of Etk/BMX obviously rescued miR-495 elevation induced inhibition of drug resistance. Etk/BMX over-expression led to higher EMT mesenchymal factors (Zeb-2, Twist, Vim) and lower epithelial molecule β-catenin, while suppression of Etk/BMX was opposite. Knockdown of Zeb-2 and Twist inhibited the chemoresistance of cells.
    
    Conclusion:
    Our study revealed that miR-495 promoted chemoresistance of SCLC through epithelial-mesenchymal transition via Etk/BMX. MiR-495 re-expression or Etk/BMX depletion is a promising strategy for interfering with chemoresistance in SCLC.
    
    

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