Your new experience awaits. Try the new design now and help us make it even better

REVIEW article

Front. Pharmacol.

Sec. Pharmacology of Anti-Cancer Drugs

This article is part of the Research TopicAdvances in Ovarian Cancer TherapeuticsView all 9 articles

Clinical relevance of PLK1 in epithelial ovarian cancer

Provisionally accepted
  • 1Capital Medical University Beijing Obstetrics and Gynecology Hospital, Beijing, China
  • 2The University of North Carolina at Chapel Hill, Chapel Hill, United States

The final, formatted version of the article will be published soon.

Ovarian cancer, particularly epithelial ovarian cancer (EOC), is the most aggressive and lethal gynecologic malignancy, necessitating the development of innovative and potent therapies to improve its prognosis. Human polo-like kinase 1 (PLK1), a key regulator of cell division, is crucial for driving mitosis and cytokinesis and maintaining genomic stability through phosphorylation of a few different substrates. PLK1 is found to be overexpressed in EOC tissues compared with normal ovarian tissues and is strongly associated with the prognosis of patients with stage I and II EOC. Targeting PLK1 markedly inhibits cell proliferation, causes cell cycle G2 phase arrest and DNA damage, induces apoptosis, and reduces tumor growth in preclinical models of EOC. In addition, the combination of PLK1 inhibitors with chemotherapeutic agents such as paclitaxel, cisplatin, doxorubicin, and PARP inhibitors exhibits effective synergistic effects in cell proliferation and tumor growth in EOC. Phase I and II clinical trials of PLK1 inhibitors in patients with EOC have shown favorable safety but inconsistent clinical efficacy. This review analyzes the existing preclinical and clinical data on PLK1 and evaluates the antitumor effects of PLK1 in EOC, offering perspectives on the potential application of PLK1 in the treatment of EOC. Keywords: PLK1, Epithelial ovarian cancer, antitumor, pre-clinical model, clinical trial.

Keywords: plk1, epithelial ovarian cancer, antitumor, Pre-clinical model, Clinical Trial

Received: 09 Sep 2025; Accepted: 26 Nov 2025.

Copyright: © 2025 Shen, Wang, Chen, Zhang, Zhou and Bae-Jump. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Chunxiao Zhou

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.