%0 Journal Article
%T KIF18B目前在癌症中的研究进展
Research Progress of KIF18B in Cancer at Present
%A 涂鸿泰
%A 肖日海
%A 刘圣银
%A 殷峰
%A 陈宏明
%J Advances in Clinical Medicine
%P 1711-1719
%@ 2161-8720
%D 2025
%I Hans Publishing
%R 10.12677/acm.2025.1541112
%X 近年来,探究KIFs家族成员在肿瘤发生和发展过程中的功能及作用机制已成为研究热点之一。驱动蛋白超家族包含一类保守的微管依赖性分子运动蛋白,具有腺苷三磷酸酶活性和运动特性。驱动蛋白的主动运动支持多种细胞功能,包括有丝分裂、减数分裂和大分子的转运。有丝分裂是真核细胞分裂的过程,涉及将细胞核、细胞质、细胞器和细胞膜分裂成2个子细胞,这些子细胞成分的部分大致相同。这个过程中的任何错误都可能导致细胞死亡、异常(如基因缺失、染色体易位或重复)和癌症。由于有丝分裂复杂且高度调节,驱动蛋白表达或功能的改变可能导致癌变。此外,由于人类癌症是一种涉及异常细胞生长的基因相关疾病,因此靶向驱动蛋白可能会为控制人类癌症创造一种新的策略。KIF18B属于驱动蛋白家族-8,近年来已经发现部分功能并证明其与多种恶性肿瘤有关。
In recent years, investigating the functions and underlying mechanisms of KIFs family members in tumorigenesis and tumor development has emerged as a prominent research area. The kinesin superfamily consists of a group of conserved microtubule-dependent molecular motor proteins, which possess adenosine triphosphatase activity and motility properties. The active motility of kinesins is crucial for supporting diverse cellular functions, such as mitosis, meiosis, and macromolecular transport. Mitosis, the process of eukaryotic cell division, involves the partitioning of the nucleus, cytoplasm, organelles, and cell membrane into two daughter cells with approximately identical components. Any aberration during this process can give rise to cell death, genetic anomalies (e.g., gene deletions, chromosomal translocations, or duplications), and cancer. Given the complexity and highly regulated nature of mitosis, changes in kinesin expression or function may trigger carcinogenesis. Moreover, as human cancer is a gene-related disorder characterized by abnormal cell growth, targeting kinesins could potentially offer a novel strategy for cancer control. KIF18B belongs to the kinesin family-8. In recent years, certain functions of KIF18B have been identified, and it has been demonstrated to be associated with various malignant tumors.
%K 驱动蛋白,
%K 驱动蛋白-8 KIF18B,
%K 癌症
Kinesin
%K Kinesin-8 KIF18B
%K Cancer
%U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=111838