由FOXM1转录调节的APOC1促进M2巨细胞两极分化和子宫癌进展
Qing Chai1, Yan Qi1, Xiaoyan Nie1
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710077, China.
Mutation research
|March 26, 2025
概括
FOXM1/APOC1轴驱动子宫癌 (CC) 的进展和M2巨细胞的两极分化. 针对这种途径为CC治疗提供了新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
背景情况:
- 宫癌 (CC) 是女性普遍存在的恶性瘤.
- M2巨细胞有助于瘤生长,转移和免疫抑制.
- 脂蛋白C1 (APOC1) 是CC中确定的瘤基因,但其在CC进展和M2巨细胞调节中的精确作用和机制需要进一步研究.
研究的目的:
- 阐明APOC1在宫癌 (CC) 进展中的作用和机制.
- 为了研究APOC1对M2巨细胞极化的影响.
- 在CC中探索APOC1和叉盒M1 (FOXM1) 之间的监管关系.
主要方法:
- 在体外测试 (CCK-8,殖民地形成,伤口愈合,transwell) 和体内小鼠模型评估了APOC1对CC细胞表型的影响.
- 定量逆转录聚合酶连锁反应 (qRT-PCR) 和流细胞计评估了M2巨细胞的两极化.
- 染色体免疫沉 (ChIP) 和 luciferase 记者测定确定了 APOC1 和 FOXM1.1 之间的相互作用.
主要成果:
- 在CC组织和细胞中,APOC1和FOXM1的表达升高.
- 击败APOC1或FOXM1抑制了CC细胞的增殖,迁移,入侵和上皮细胞-介质细胞过渡 (EMT),并减弱了M2巨细胞的两极分化.
- 在体内,FOXM1转录激活APOC1和APOC1过度表达抵消了FOXM1的淘汰效应;APOC1淘汰减少了瘤生长和M2极化.
结论:
- FOXM1/APOC1轴促进子宫癌 (CC) 的进展.
- 这个轴在调节M2巨细胞极化方面发挥着至关重要的作用.
- FOXM1/APOC1通路为CC治疗提供了一个有前途的治疗标.
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