Silva João P N, Silva Patrícia M A, Bousbaa Hassan
UNIPRO-Oral Pathology and Rehabilitation Research Unit, University Institute of Health Sciences (IUCS), Cooperativa de Ensino Superior Politécnico e Universitário (CESPU), 4585-116 Gandra, Portugal.
Associate Laboratory i4HB-Institute for Health and Bioeconomy, University Institute of Health Sciences-CESPU, 4585-116 Gandra, Portugal.
Int J Mol Sci. 2025 Sep 15;26(18):8975. doi: 10.3390/ijms26188975.
Kinesin spindle protein (KSP), also known as KIF11, is a member of the kinesin superfamily of motor proteins that plays a pivotal role in mitosis by regulating spindle assembly, chromosome alignment, and segregation. Its motor activity, which is essential for the proper organization of microtubules during mitosis, is crucial for maintaining genomic stability. KSP overexpression has been observed in several cancer types, where it promotes uncontrolled cell proliferation, making it a promising target for cancer therapy. This review provides a comprehensive analysis of the molecular mechanisms underlying KSP function, including its structural features, ATPase activity, and interactions with other mitotic proteins. Additionally, we review the regulation of KSP through post-translational modifications, such as phosphorylation, as well as the therapeutic strategies currently being explored to inhibit its activity in cancer treatment.
驱动蛋白纺锤体蛋白(KSP),也称为KIF11,是驱动蛋白超家族运动蛋白的成员,通过调节纺锤体组装、染色体排列和分离在有丝分裂中起关键作用。其运动活性在有丝分裂期间对微管的正确组织至关重要,对维持基因组稳定性至关重要。在几种癌症类型中已观察到KSP过表达,它促进不受控制的细胞增殖,使其成为癌症治疗的一个有前景的靶点。本综述对KSP功能的分子机制进行了全面分析,包括其结构特征、ATP酶活性以及与其他有丝分裂蛋白的相互作用。此外,我们还综述了通过翻译后修饰(如磷酸化)对KSP的调节,以及目前正在探索的在癌症治疗中抑制其活性的治疗策略。