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Oncogenesis. 2017 Jul 31;6(7):e366. doi: 10.1038/oncsis.2017.66.

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

Author information

1
Department of Molecular Biology and Biochemistry, Francisco J. Ayala School of Biological Sciences, University of California, Irvine, CA, USA.
2
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
3
Department of Pathology, Aarhus University Hospital, Aarhus, Denmark.
4
Department of Pathology, Vejle Hospital, Vejle, Denmark.
5
Department of Molecular Medicine, Aarhus University Hospital, Aarhus, Denmark.
6
Departments of Neurology, Pathology and Cell Biology, Pharmacology, Columbia University Medical Center, New York, NY, USA.

Abstract

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.

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