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在巨细胞中缺少伴侣介导的自会加剧大肠炎和大肠炎相关的瘤发生在小鼠中

Weichun Zhu¹, Zehao Chen¹, Yunqian Gao¹

¹State Key Laboratory for Innovation and Transformation of Luobing Theory, Qilu Hospital of Shandong University, Jinan, China, 250012; Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Qilu Hospital of Shandong University, Jinan, China, 250012; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China, 250012.

Molecules and cells

|November 14, 2025

概括

与瘤相关的巨细胞中Chaperone介导的自 (CMA) 缺乏会使结直肠癌 (CRC) 恶化. 在这些巨细胞中恢复CMA可抑制CRC进展和血管生成,这表明CMA是治疗点.

科学领域:

细胞生物学细胞生物学
癌症研究癌症研究
免疫学免疫学免疫学

背景情况:

沙波龙介导的自 (CMA) 降解 lysosomes 中的细胞质蛋白质.
CMA与结直肠癌 (CRC) 有关,但其在瘤相关巨细胞 (TAMs) 中的作用尚未得到充分研究.
LAMP2A是CMA的速度限制蛋白.

研究的目的:

研究巨细胞CMA在结肠炎和CRC中的作用.
为了确定LAMP2A表达在巨细胞对CRC发育和进展的影响.

主要方法:

产生了特定于骨髓细胞的LAMP2A敲除和敲进小鼠.
使用德克斯硫酸盐 (DSS) 诱导的大肠炎和阿佐西甲/DSS诱导的CRC模型.
分析了人类和小鼠CRC组织和TAM中的LAMP2A表达.

主要成果:

人和小鼠CRC的TAMs中的LAMP2A表达减少了.
在巨细胞中LAMP2A淘汰会加剧结肠炎和CRC;过度表达会减轻它.
通过对HIF-1α,VEGF-A和IL-1β进行上调,LAMP2A缺乏会增加血管生成.

结论:

巨细胞CMA在调节大肠炎和CRC方面发挥着关键作用.
向巨细胞CMA激活为CRC提供了潜在的治疗策略.

关键词:

血管新生的产生.陪伴者介导的自细胞.结肠直肠癌是一种癌症.低氧诱导因子1α 与瘤相关的巨细胞.

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