miR-151a induces partial EMT by regulating E-cadherin in NSCLC cells

Research output: Research - peer-reviewJournal article

DOI

  • Iben Daugaard
  • K J Sanders
    K J SandersDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • A Idica
    A IdicaDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • K Vittayarukskul
    K VittayarukskulDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • M Hamdorf
    M HamdorfDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • J D Krog
    J D KrogDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • R Chow
    R ChowDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • D Jury
    D JuryDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • L L Hansen
  • H Hager
  • P Lamy
  • C L Choi
    C L ChoiDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
  • D Agalliu
    D AgalliuDepartments of Neurology, Pathology and Cell Biology, Pharmacology, Columbia University Medical Center, New York, NY, USA.
  • D G Zisoulis
    D G ZisoulisDepartment of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.

miR-151a and its host gene, focal adhesion kinase, FAK, are located in a region of chromosome 8q that is frequently amplified in solid tumors, including lung cancer. Lung cancer is the leading cause of cancer deaths worldwide and metastasis remains the major challenge in battling lung cancer mortality. Here, we demonstrate that miR-151a is overexpressed in non-small cell lung cancer (NSCLC) patient specimens, as compared to healthy lung. In addition, miR-151a overexpression promotes proliferation, epithelial-to-mesenchymal transition (EMT) and induces tumor cell migration and invasion of NSCLC cells. Blocking miR-151a expression using anti-miR-151a approaches significantly reduced NCSLC cell proliferative and motility potential. Furthermore, we determined that miR-151a significantly regulates E-cadherin expression. Finally, functional rescue experiments determined that overexpression of E-cadherin in miR-151a NSCLC cell lines potently repressed miR-151a-induced partial EMT and cell migration of NSCLC cells. In conclusion, our findings suggest that miR-151a functions as an oncomiR in NSCLC by targeting E-cadherin mRNA and inducing proliferation, migration and partial EMT.

Original languageEnglish
JournalOncogenesis
Volume6
Issue number7
Pages (from-to)e366
ISSN2157-9024
DOIs
StatePublished - 31 Jul 2017

    Research areas

  • Journal Article

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