The Roles of E2F5 in Tumor Cell Cycle: The Gatekeeper or Destroyer?

¹ Department of Urology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China; The First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China,

² Department of Urology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong, China; Guangdong Engineering Research Center of Commercialization of Medical Institution Preparations and Traditional Chinese Medicines, Guangzhou, Guangdong, China; Guangdong Engineering Technology Research Center of Commercialization of Lingnan Special Medical Institution Preparations, Guangzhou, Guangdong, China; The First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China,

³ The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China,

UR 2025 , 3(3), 13–24; https://doi.org/10.26689/ur.v3i3.12411

© 2025 by the Authors. Licensee Whioce Publishing, Singapore. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )

Abstract

E2F5 is a member of E2F transcription factor superfamily, controlling many molecular activities, such as cell proliferation, cell differentiation, DNA repair and cell death. Therefore, it is closely related to the occurrence, development and prognosis of a variety of cancers. In recent years, with the rapid development of bioinformatics, genomics and epigenetics, this study has further elucidated of E2F5 in the tumor cell cycle. Based on the latest research reports, this study reviewed the structural composition, dynamic activity regulation of E2F5, and how its transcription program driven by carcinogenic activity changed the progress of various tumor cell cycles, especially how it converted from a “gatekeeper” to a “destroyer”, thus affecting abnormal biological behaviors of tumor cells. Our aim is to provide a new direction for the development of E2F5 targeted therapy strategies and drug resistance in the future.

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