Background: Polo-like kinase 1 (PLK1) is a serine/threonine protein kinase, which has been studied as a potential gene therapy target for many years. PLK1 is overexpressed in a variety of tumors, and its expression often negatively correlated with patient prognosis. However, the role of PLK1 in nasopharyngeal carcinoma (NPC) is rarely studied.
Methods: Two recombinant vector plasmids were transfected into CNE2 cell lines by liposome transfection, CNE2/PLK1 shRNA target PLK1 mRNA, as well as a non-targeting control plasmid, CNE2/NC shRNA. Meanwhile, non-transfected cells (CNE2) were also used as controls. Real-time quantitative PCR (qRT-PCR) and Western blotting were performed to detect the transfection effect. The effects of the downregulation of PLK1 on cell biological behavior was evaluated in vitro by using CCK8, Transwell, colony-forming and flow-cytometry assays.
Results: PLK1 mRNA and protein were significantly inhibited in CNE2/PLK1 shRNA cells. Compared to control groups, the CNE2/PLK1 shRNA cells showed slower cell growth and a significantly decreased cell-cloning rate. Both migration and invasion were significantly inhibited in experimental cells. The proportions of G2-phase and apoptotic cells within the experimental group were significantly increased.
Conclusions: Our results indicate that specific interference of PLK1 gene expression can significantly inhibit the proliferation and invasion of NPC (CNE2) cells.
Keywords: Polo-like kinase 1 (PLK1); biological behavior; down-regulation; nasopharyngeal carcinoma (NPC); targeted therapy.
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