Polo‑like kinase 3 inhibits osteosarcoma cell proliferation and tumorigenesis via cooperative interaction with p21

Molecular Medicine Reports
Honglin LvYujie Sun

Abstract

Polo‑like kinase 3 (Plk3) is a member of the Plk family. It is dysregulated in certain types of cancer, including colorectal and pancreatic cancer. However, the expression status and biological function of Plk3 in osteosarcoma (OS) remain poorly understood. Following evaluation of the role of Plk3 in OS, the present study indicates that Plk3 is downregulated in OS cell lines and tissues, and increased expression levels of Plk3 are associated with improved rates of overall survival of patients. In addition, to investigate the role of Plk3 in cell proliferation and tumorigenicity in vitro, two recombinant lentiviruses expressing Plk3 short hairpin RNA, as well as a recombinant plasmid carrying Plk3, were developed and transfected into Saos‑2 and U2OS cells, respectively. Cell cycle analysis by flow cytometry demonstrated the influence of Plk3 on the arrest of cell cycle progression at the G1 phase. Following knock down of Plk3, the growth and colony formation of Saos‑2 cells increased significantly, whereas the overexpression of Plk3 resulted in the opposite trend. Furthermore, a 5‑ethynyl‑2'‑deoxyuridine assay, using U2OS cell lines, indicated the same tendency. The in vivo interaction between Plk3 and p21 in Saos‑2 cells was de...Continue Reading

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