驱动蛋白KIF23在恶性肿瘤中的研究进展
Research Progress of Kinesin KIF23 in Malignant Tumors
DOI: 10.12677/acm.2026.1651934, PDF,   
作者: 何 郡*：右江民族医学院研究生学院，广西 百色；孙文忠#：广西科技大学医学部，广西 柳州
关键词: 驱动蛋白KIF23；恶性肿瘤；分子机制；靶向治疗；肿瘤微环境；Kinesin KIF23； Malignant Tumors； Molecular Mechanisms； Targeted Therapy； Tumor Microenvironment
摘要: KIF23作为kinesin-6家族核心成员，通过调控胞质分裂和信号通路重编程在恶性肿瘤发生发展中发挥关键作用。本综述系统阐述了KIF23的分子机制，聚焦KIF23在多种实体瘤中的异常高表达及其与患者预后的显著相关性，论证其作为新兴治疗靶点的潜力。同时，深入探讨靶向KIF23的小分子抑制剂开发、耐药机制及联合免疫治疗的策略挑战，为未来转化研究提供理论依据。最后强调非编码RNA介导的KIF23调控网络在肿瘤微环境重塑中的前沿进展，指明跨学科研究对突破临床瓶颈的重要性。
Abstract: KIF23, a core member of the kinesin-6 family, exerts pivotal functions in malignant tumorigenesis and progression through orchestrating cytokinesis and signal transduction pathway reprogramming. This review systematically delineates the molecular mechanisms underlying KIF23 activity, with particular emphasis on its aberrant overexpression across diverse solid malignancies and the significant correlation with patient prognosis, substantiating its emerging potential as a therapeutic target. Furthermore, we critically examine the developmental landscape of small-molecule inhibitors targeting KIF23, elucidate underlying resistance mechanisms, and address strategic challenges in combinatorial immunotherapeutic approaches, thereby furnishing theoretical foundations for future translational investigations. Finally, we highlight frontier advances in non-coding RNA-mediated regulatory networks of KIF23 within tumor microenvironment remodeling, underscoring the imperative of interdisciplinary research in surmounting clinical bottlenecks.
文章引用：何郡, 孙文忠. 驱动蛋白KIF23在恶性肿瘤中的研究进展[J]. 临床医学进展, 2026, 16(5): 1331-1339. https://doi.org/10.12677/acm.2026.1651934

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