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

Lv,Honglin; Gao,Guangting; Zhang,Linlin; Sun,Yujie

doi:10.3892/mmr.2015.4304

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

Authors:
- Honglin Lv
- Guangting Gao
- Linlin Zhang
- Yujie Sun
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Affiliations: Department of Spinal Orthopedics, Yantai Yuhuangding Hospital Affiliated to Qingdao University Medical College, Yantai, Shandong 264000, P.R. China, Department of Bone Surgery, Binzhou Central Hospital, Binzhou, Shandong 251700, P.R. China, Department of Orthopedics, The People's Hospital of Gaomi, Gaomi, Shandong 261500, P.R. China
Published online on: September 9, 2015 https://doi.org/10.3892/mmr.2015.4304
Pages: 6789-6796

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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 detected and the protein level of p21 was observed to be consistent with that of Plk3. These results imply that Plk3 is involved in the inhibition of cell proliferation and tumorigenesis, which may occur via interactions with p21, thus, Plk3 may be considered as a potential candidate for targeted therapy of OS.

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