通过S100A8/A9-MCAM信号传递,通过ERK-c-Jun激活促进胃癌细胞的进展
Youyi Chen1, Xu Yang2, Rie Kinoshita3
1Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China. chenyouyi86@163.com.
In vitro cellular & developmental biology. Animal
|September 9, 2025
概括
蛋白质复合体S100A8/A9通过结合其受体,黑色素瘤细胞粘附分子 (MCAM) 来促进胃癌 (GC) 的进展. 这种相互作用激活ERK-c-Jun通路,驱动瘤生长和转移.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- S100蛋白家族成员S100A8和S100A9形成一个异构体 (S100A8/A9),在各种癌症中至关重要.
- 胃癌 (GC) 的发病包括瘤的进展,炎症和转移,其中S100A8 / A9涉及但机制不清楚.
研究的目的:
- 研究S100A8/A9复合体及其受体在胃癌进展中的作用.
- 阐明涉及S100A8/A9介导的GC病变发生的分子信号通路.
主要方法:
- 黑色素瘤细胞粘附分子 (MCAM) 在GC组织中的表达的免疫组织化学分析.
- 在体外穿孔迁移和入侵试验测试以评估GC细胞运动性.
- 细胞增殖测定和西部抹杀检查ERK和c-Jun信号通路.
主要成果:
- 通过S100A8/A9刺激,通过MCAM结合显著增强GC细胞的增殖和迁移.
- MCAM激活导致下游ERK酸化和c-Jun诱导.
- 下调MCAM废除了ERK酸化和c-Jun表达,证实了S100A8/A9―MCAM―ERK―c-Jun轴.
结论:
- S100A8/A9通过MCAM介导的ERK-c-Jun信号通路的激活来促进胃癌的进展.
- S100A8/A9-MCAM信号轴代表了胃癌治疗的潜在新型治疗标.
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