Abstract
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. Plk1 has been closely linked to cellular proliferation, cancer development and cancer progression. There is no Plk1 expression in most differentiated cells in contrast to tissues with proliferative potential such as placenta and cancers. Many studies have shown that Plk1 expression is strongly correlated with aggressiveness and prognosis in gynecologic cancers. Plk1 gene and protein expression has been proposed as a new prognostic marker for gynecologic malignancies, and Plk1 is a potential target for cancer therapy. To date, several techniques and compounds to inhibit Plk1 have been identified and appear to be promising. In the future, methods for inhibition of Plk1 could be improved and applied in treatment of cancer patients.
Keywords: Polo-like kinases, ovarian cancer, endometrial cancer
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