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RUNX1通过ACP5/SMAD3介导的M2巨细胞极化促进NSCLC的进展

Changjun He¹, Yingbin Li², Nianyu Gao³

¹Department of Thoracic Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, 150086, Heilongjiang, China. ChangjunHe1209@163.com.

Inflammation research : official journal of the European Histamine Research Society ... [et al.]

|November 6, 2025

概括

RUNX1通过通过ACP5和β-catenin增强M2巨分极,从而促进肺癌的进展,从而导致SMAD3酸化的增加. 抑制RUNX1抑制了小鼠的瘤生长.

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:

与瘤相关的巨细胞 (TAMs) 在瘤微环境中起着至关重要的作用.
大细胞两极分化,特别是M2两极分化,与癌症的进展和免疫逃避有关.
转录因子RUNX1 (与Runt相关的转录因子1) 已与各种癌症有关,但其在调节肺癌中TAMs的具体作用尚不清楚.

研究的目的:

研究RUNX1调节肺癌中瘤相关巨细胞 (TAMs) M2极化机制.
阐明涉及RUNX1-介导的巨细胞两极化及其对非小细胞肺癌 (NSCLC) 进展的影响下游信号通路.

主要方法:

骨髓衍生巨细胞 (BMDMs) 用瘤条件介质 (CM) 进行刺激,并用RUNX1shRNA,pCDNA3.1-ACP5或SIS3.3.5进行治疗.
使用流式细胞计和ELISA分析了巨分极和细胞因子分泌.
评估了RUNX1,ACP5,p-β-catenin,β-catenin和p-SMAD3中的蛋白质水平. 通过共同免疫沉 (Co-IP) 证实了ACP5和β-catenin之间的相互作用.
共同培养系统 (Transwell) 和体内小鼠模型 (路易斯肺癌) 用于评估对癌细胞恶性和瘤生长的影响.

主要成果:

瘤CM诱导了BMDM中的M2极化,M2型巨细胞中RUNX1表达上调.
RUNX1 knockdown 将巨细胞转移到M1偏向,减少M2标记物,并抑制NSCLC细胞恶性病变.
通过增强ACP5-β-catenin相互作用,RUNX1促进了M2极化和NSCLC的进展,导致SMAD3酸化的增加. 在体内,RUNX1敲击抑制了M2极化和瘤生长.

结论:

在肺癌的瘤微环境中,RUNX1驱动着巨细胞的M2极化.
这一过程通过促进ACP5和β-catenin之间的相互作用来调解,随后增加SMAD3的酸化.
RUNX1诱导的M2极化有助于非小细胞肺癌 (NSCLC) 的进展,突出了RUNX1作为潜在的治疗点.

关键词:

在ACP5 ACP5中,这是入侵.巨细胞是一个巨细胞.移民移民移民非小细胞肺癌的非小细胞肺癌.在RUNX1中,使用RUNX1.在SMAD3中,我们可以看到SMAD3.

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