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CTSZ-TRA2A-IL32轴定义了转移性前列腺癌中可向的巨细胞依赖途径

Saipeng Chen¹, Bingqian Deng², Youxin Liu¹

¹Department of Urology, Southwest Hospital, Army Medical University (Third Military Medical University), GaoTanYan Main Street 30, Chongqing, 400038, China.

Journal of translational medicine

|August 6, 2025

概括

CTSZ/TRA2A/IL-32/ITGA5通路驱动M2-TAM的招募,促进前列腺癌的转移. 用GLPG0187抑制整合素α-5 (ITGA5) 减少转移并重塑瘤微环境.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

M2极化瘤相关巨细胞 (M2-TAMs) 促进免疫抑制的瘤微环境,促进前列腺癌 (PCa) 转移.
在致命的PCa进展中,M2-TAM贩运的机制尚未完全理解.

研究的目的:

阐明管理前列腺癌转移中的M2-TAM贩运的分子机制.
确定抑制PCa转移传播的治疗点.

主要方法:

转录组分析以确定转移相关的基因,优先考虑CTSZ.
在体内小鼠模型 (循环瘤和骨转移) 研究CTSZ驱动的M2-TAM透.
关于蛋白质体降解,IL32剪接和整体素结合的机制研究.
对ITGA5抑制剂GLPG0187.7.的临床前测试

主要成果:

升高的CTSZ表达与先进的PCa相关,并驱动肺和骨转移.
过度表达CTSZ通过诱导TRA2A降解来促进M2-TAM透,减轻IL32拼接抑制.
增加的IL-32分泌通过整体蛋白ITGA5.5招募M2-TAMs.
GLPG0187治疗显著降低了转移负担和M2-TAM透.

结论:

CTSZ/TRA2A/IL-32/ITGA5轴通过驱动M2-TAM招募来协调PCa转移中的突性免疫力.
向ITGA5提供了一个有前途的治疗策略,以抑制PCa转移并重塑瘤微环境.

关键词:

在CTSZZ中.对于IL-32来说,它是非常重要的.在ITGA5中,它是ITGA5.巨细胞是一个巨细胞.在TRA2A中.瘤微环境是一个微环境.

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