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在调节GBM恶性转变中的ICAM1-介导的内皮细胞和巨相互作用

Junlin Li^1,2, Tingyu Liang¹, Bo Liang^3,4

¹Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.

Journal of inflammation research

|November 11, 2025

概括

复发性质母细胞瘤涉及低氧驱动的反循环,其中内皮细胞上调ICAM1,招募巨细胞. 然后,来自巨细胞的ADM促进瘤生长和血管生成.

科学领域:

在瘤学瘤学.
癌症生物学癌症生物学
免疫学免疫学免疫学

背景情况:

质母细胞瘤 (GBM) 经常复发,在脑瘤治疗中构成重大挑战.
内皮细胞是原发性GBM中瘤微环境 (TME) 的关键组成部分,但它们在复发性GBM (rGBM) 中的具体作用尚不清楚.

研究的目的:

为了研究内皮细胞在瘤微环境中的反复性质母细胞瘤的作用.
确定驱动GBM复发和潜在治疗点的分子机制.

主要方法:

从GBM患者数据中对内皮细胞的单细胞RNA测序分析.
差异基因表达和伪时间轨迹分析以确定关键基因.
TCGA数据验证,免疫光,基因淘汰和共同培养实验,以探索细胞交叉通话.

主要成果:

确定了两个不同的内皮细胞群,其中一个与rGBM的预后较差有关.
细胞间粘附分子-1 (ICAM1) 被确定为由rGBM内皮细胞中缺氧升高调节的关键基因,促进巨细胞的招募.
观察到一个反循环,其中内皮衍生CCL2诱导的巨细胞衍生上腺素 (ADM),促进血管生成和瘤细胞增殖/迁移.

结论:

在内皮细胞中因缺氧诱导的ICAM1上调有助于对rGBM的巨细胞的招募.
由CCL2和ADM介导的内皮细胞-巨细胞交叉,在rGBM微环境中创建了一个亲瘤循环.
这些发现提供了对rGBM进展的机制性见解,并建议针对这一轴的潜在治疗策略.

关键词:

上腺素上腺素上腺素内皮细胞是内皮细胞.质母细胞瘤 (glioblastoma) 是一种细胞间粘附分子 1 细胞间粘附分子 1

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