Polo-like kinases (Plks) and cancer

• Published in: Oncogene Vol. 24; no. 2; pp. 287 - 291
• Main Authors: Takai, Noriyuki, Hamanaka, Ryoji, Yoshimatsu, Jun, Miyakawa, Isao
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 10-01-2005
• Subjects: Animals; Cancer; Cell cycle; Cell Cycle Proteins; Centrosome - physiology; Chromosomes; DNA damage; Humans; Kinases; Medical prognosis; Neoplasms - enzymology; Phosphorylation; Polo-Like Kinase 1; Protein Kinases - physiology; Protein Serine-Threonine Kinases - physiology; Proteins; Proto-Oncogene Proteins; Tumor Suppressor Proteins; Tumors; University faculty; Yeast
• ISSN: 0950-9232; 1476-5594
• DOI: 10.1038/sj.onc.1208272

Deregulated centrosome duplication or maturation often results in increased centrosome size and/or centrosome number, both of which show a positive and significant correlation with aneuploidy and chromosomal instability, thus contributing to cancer formation. Given the role of Polo-like kinases (Plks) in the centrosome cycle, it is not unexpected that deregulated expression of Plks is detected in many types of cancer and is associated with oncogenesis. Extensive studies have shown that Plk1 expression is elevated in non-small-cell lung cancer, head and neck cancer, esophageal cancer, gastric cancer, melanomas, breast cancer, ovarian cancer, endometrial cancer, colorectal cancer, gliomas, and thyroid cancer. Plk1 gene and protein expression has been proposed as a new prognostic marker for many types of malignancies, and Plk1 is a potential target for cancer therapy. In contrast to Plk1, several studies have observed that Plk3 expression is negatively correlated with the development of certain cancers.