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Oncol Rep. 2016 Jan;35(1):497-503. doi: 10.3892/or.2015.4392. Epub 2015 Nov 4.

miR-296-5p suppresses cell viability by directly targeting PLK1 in non-small cell lung cancer.

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Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Department of Thoracic Surgery, Taicang Affiliated Hospital of Soochow University, Taicang, Jiangsu 215400, P.R. China.
Department of Respiratory Medicine, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
Suzhou Key Laboratory for Cancer Molecular Genetics, Suzhou, Jiangsu 215123, P.R. China.


Polo-like kinase 1 (PLK1), a critical kinase for mitotic progression, is overexpressed in a wide range of cancers. MicroRNAs (miRNAs) are a class of small non-coding RNA molecules and proposed to play important roles in the regulation of tumor progression and invasion. However, the relationship between PLK1 and miRNAs have remained unclear. In the present study, the association between PLK1 and miR-296-5p was investigated. The upregulation of PLK1 mRNA expression levels combined with the downregulation of miR-296-5p levels were detected in both non-small cell lung cancer (NSCLC) tissues and cell lines. Functional studies showed that knockdown of PLK1 by siRNA inhibited NSCLC cells proliferation. Impressively, overexpression of miR-296-5p showed the same phenocopy as the effect of PLK1 knockdown in NSCLC cells, indicating that PLK1 was a major target of miR-296-5p. Furthermore, using western blot analysis and luciferase reporter assay, PLK1 protein expression was proved to be regulated by miR-296-5p through binding to the putative binding sites in its 3'-untranslated region (3'-UTR). Taken together, the present study indicated that miR-296-5p regulated PLK1 expression and could function as a tumor suppressor in NSCLC progression, which provides a potential target for gene therapy of NSCLC.

[Indexed for MEDLINE]

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