The molecular aspects in prostatic cancer, unraveling the role of CDKs in prostate cancer progression

Zahra Farjami; Zahra Mohammadzadeh; Bita Saifi; Mahasti Tavakoli Nezhad; Mohammad Mehdi Akbarin

doi:10.1007/s12672-025-03605-w

The molecular aspects in prostatic cancer, unraveling the role of CDKs in prostate cancer progression

Discov Oncol. 2025 Oct 15;16(1):1900. doi: 10.1007/s12672-025-03605-w.

Authors

Zahra Farjami¹, Zahra Mohammadzadeh², Bita Saifi³, Mahasti Tavakoli Nezhad⁴, Mohammad Mehdi Akbarin^{5

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Affiliations

¹ Department of Modern Sciences and Technologies, Faculty of Medicine, Mashhad University of Medical, Mashhad, Iran.
² School of Health, Vancouver Career College, Burnaby, BC, Canada.
³ Department of Anatomy, Faculty of Medicine, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Iran.
⁴ Department of Medical Laboratory Sciences, Mashhad Branch, Islamic Azad University, Mashhad, Iran.
⁵ Biological Sciences Department, Facultad de Estudios Superiores Cuautitlán-UNAM, Mexico City, Mexico. Akbarinmm@iau.ac.ir.
⁶ Basic Sciences Department, Medical School, Mashhad Medical Sciences, Islamic Azad University, Mashhad, Iran. Akbarinmm@iau.ac.ir.
⁷ Immunology Department, Mashhad University of Medical Sciences, Medical School, Mexico City, Mexico. Akbarinmm@iau.ac.ir.

Abstract

Background: Prostate cancer (PCa) is one of the leading causes of morbidity and mortality in the world, it becomes imperative to investigate the molecular mechanisms underlying practical therapeutic approaches. Cyclin-dependent kinases (CDKs) are critical regulators of cell cycle progression, and their dysregulation has been implicated in PCa.

Methods: This review synthesizes recent findings on CDK-mediated signaling pathways and their role in PCa progression. The overall goal of this review article is to elucidate the molecular mechanisms by which CDK molecules contribute to the development, progression, and metastasis of PCa.

Results: Elevated expression of CDK1, CDK3, CDK5, and CDK16 is associated with poorer outcomes, and specifically, high CDK3 expression correlates with shorter progression-free survival.

Conclusions: Targeting CDKs, particularly CDK3 and CDK4/6, may represent a promising therapeutic strategy for PCa.

Keywords: CDK; Cell cycle inhibitors; Cyclins; Molecular pathogenesis; Prostate cancer.

Publication types

Review