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干细胞CD24激活促进肝细胞癌的进展通过免疫逃生机制

Yin Cai¹, Lu-Yin Liu², Xiao-Xiao Xia³

¹Department of Oncology, Xinghua People's Hospital, Xinghua 225700, Jiangsu Province, China.

World journal of gastroenterology

|February 5, 2026

概括

差异化集群24 (CD24) 通过编程死亡配体1 (PD-L1) 信号传递促进肝细胞癌 (HCC). 升高的CD24是监测肝病恶性和HCC进展的潜在生物标志物.

科学领域:

肝病学和癌症研究研究.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

分化24集群 (CD24) 与肝癌干细胞活性和慢性肝病进展有关.
CD24在肝癌发生中的确切作用需要进一步阐明.

研究的目的:

在患有慢性肝病的患者中评估CD24水平.
调查大鼠肝癌发生过程中CD24和编程死亡配体1 (PD-L1) 表达的动态变化.

主要方法:

在患有肝细胞癌 (HCC),慢性肝炎 (CH),肝硬化 (LC) 和正常对照 (NC) 的患者中测量了血清CD24水平.
用接收器操作特征 (ROC) 曲线评估CD24的诊断和预后值.
在大鼠HCC模型中分析了CD24+T细胞比率和动态CD24/PD-L1表达.

主要成果:

与CH,LC和NC组相比,在HCC患者中观察到显著更高的CD24水平和CD24+T细胞比例.
高CD24表达在HCC与先进的临床病理特征相关,包括转移和不良预后.
在肝癌发生过程中CD24的上调与PD-L1,免疫逃逸,转移标志物 (CD44) 和HCC标志物 (Wnt3a,GPC-3,alpha-fetoprotein) 有正相关.

结论:

激活的CD24通过PD-L1信号驱动HCC的发展.
CD24是监测慢性肝病和HCC恶性瘤的一个有前途的生物标志物.

关键词:

生物标志物生物标志物慢性肝病是一种慢性肝病.差异化的集群 24 差异化的集群肝癌的发生是肝癌的产生.编程死亡联手 1 编程死亡联手 1

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