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Cell cycle regulator proteins are a broad class of molecules, including cyclin-dependent kinases (CDKs), cyclins, and CDK inhibitors, that orchestrate the orderly progression of cells through the growth and division phases (G1, S, G2, and M) [1]. These proteins function as essential checkpoints, ensuring that critical processes like DNA replication and chromosome segregation are completed accurately before the cell proceeds to the next stage [4]. Dysregulation of these regulators is a fundamental hallmark of cancer, where loss of control leads to unchecked cell proliferation and genomic instability [2]. Consequently, many proteins within this class have become significant therapeutic targets, particularly in oncology, where drugs are designed to restore cell cycle control or induce arrest in malignant cells [3]. For example, CDK4/6 inhibitors have revolutionized the treatment of certain breast cancers by blocking the transition from the G1 to the S phase [3]. Other agents target the mitotic spindle or DNA damage response pathways to exploit vulnerabilities in the cell cycle machinery [2]. However, because these proteins are also active in normal dividing cells, therapeutic intervention can lead to side effects such as myelosuppression and gastrointestinal distress [2]. Understanding the complex interplay between these regulators is crucial for developing more selective and effective therapies [1].
Inhibition of cyclin-dependent kinases (CDKs) to induce cell cycle arrest, stabilization of microtubules to inhibit mitosis, and modulation of checkpoint proteins to trigger apoptosis in rapidly dividing cells.
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