驱动蛋白家族成员18B在子宫内膜癌中的作用机制与分子分型关联分析

doi:10.12280/gjfckx.20260137

摘要/Abstract

摘要：

目前子宫内膜癌（endometrial cancer，EC）的发病率持续上升，严重威胁女性健康，传统分型与治疗手段面临挑战。驱动蛋白家族成员18B（kinesin family member 18B，KIF18B）作为驱动蛋白超家族蛋白成员之一，在细胞有丝分裂与染色体分离中起核心作用。KIF18B在包括EC在内的多种恶性肿瘤中异常高表达，其表达水平与EC患者的不良临床病理特征及更差的总体生存期显著相关，KIF18B在分子机制上通过激活Wnt/β-联蛋白（β-catenin）、PI3K/Akt/mTOR等信号通路调控细胞周期进程，诱导上皮-间质转化（epithelial-mesenchymal transition，EMT），维持肿瘤干细胞特性，并参与塑造免疫抑制性肿瘤微环境，从而协同驱动EC的发生与发展。随着EC分子分型在临床实践中的普及，KIF18B在不同分子亚型的潜在关联为其作为预后预测生物标志物和亚型特异性治疗靶点提供了新的视角。基于KIF18B调控染色体分离的核心功能及其同源蛋白KIF18A在染色体不稳定性（chromosomal instability，CIN）细胞中的选择性致死证据，KIF18B在p53异常（p53-abnormal，p53abn）型中可能具有靶点潜力，在错配修复缺陷（mismatch repair-deficient，MMRd）型中则可能通过重塑免疫微环境影响免疫检查点抑制剂疗效。系统综述了KIF18B的生物学特性、在EC中的表达调控网络、促癌分子机制及其与EC分子分型的潜在关联，并探讨了其临床转化面临的挑战与未来方向，旨在为EC的精准诊断与靶向治疗提供新的理论依据和研究思路。

关键词: 驱动蛋白家族成员18B, 子宫内膜肿瘤, 癌, 分子机制, 分子分型, 染色体不稳定性

Abstract:

The incidence of endometrial cancer (EC) continues to rise, posing a serious threat to women's health and challenging conventional classification and treatment approaches. Kinesin family member 18B (KIF18B), as a member of the kinesin superfamily, plays a pivotal role in mitotic cell division and chromosome segregation. KIF18B is aberrantly overexpressed in various malignancies, including EC, and its expression level is significantly correlated with adverse clinicopathological features and worse overall survival in EC patients. Mechanistically, KIF18B regulates cell cycle progression by activating signaling pathways such as Wnt/β-catenin and PI3K/Akt/mTOR, induces epithelial-mesenchymal transition (EMT), maintains cancer stem cell properties, and participates in shaping an immunosuppressive tumor microenvironment, thereby synergistically driving the initiation and progression of EC. With the increasing adoption of EC molecular classification in clinical practice, the potential association of KIF18B with different molecular subtypes offers novel perspective for its application as a prognostic biomarker and a subtype-specific therapeutic target. Based on the core function of KIF18B in chromosome segregation and the evidence for selective lethality of its homologous protein KIF18A in chromosomally unstable (CIN) cells, KIF18B may harbor targeting potential in the p53-abnormal（p53abn） subtype, and it could influence the efficacy of immune checkpoint inhibitors by remodeling the immune microenvironment in the mismatch repair-deficient（MMRd） subtype. This review systematically summarizes the biological characteristics, of KIF18B, its expression regulatory network and oncogenic mechanisms in EC, its potential association with EC molecular subtypes, and discusses the challenges and future directions for its clinical translation, aiming to provide a novel theoretical foundations and research direction for the precise diagnosis and targeted therapy of EC.

Key words: Kinesin family member 18B, Endometrial neoplasms, Carcinoma, Molecular mechanisms, Molecular subtyping, Chromosomal instability

王薇, 戴柏, 沙日娜, 托娅. 驱动蛋白家族成员18B在子宫内膜癌中的作用机制与分子分型关联分析[J]. 国际妇产科学杂志, 2026, 53(3): 292-297.

WANG Wei, DAI Bai, SHA Ri-na, TUO Ya. Analysis of the Role and Molecular Subtype Association of Kinesin Family Member 18B in Endometrial Carcinoma[J]. Journal of International Obstetrics and Gynecology, 2026, 53(3): 292-297.

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