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杆菌有助于GC的进展,可能通过MSTRG.10627.1/miR-142-5p/ADAMTS5路径
Zhipeng Yin1,2, Jianwei Xiang3, Pengbo Guo1,2
1Laboratory of Metabolism and Gastrointestinal Tumor, The First Affiliated Hospital of Shandong First Medical University, Jinan, Shandong, China.
杆菌降低ADAMTS5的调节,促进胃癌 (GC) 细胞的增殖和转移. 这项研究阐明了MSTRG.10627.1/miR-142-5p/ADAMTS5途径参与H. pylori诱导的GC.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 微生物学 微生物学
背景情况:
- 杆菌 (H. pylori) 是一种与胃癌 (GC) 相关的I类致癌物.
- 人们对H. pylori诱导GC的精确分子机制尚不完全了解.
- 这项研究调查了MSTRG.10627.1/miR-142-5p/ADAMTS5通路在H. pylori介导的GC病变发生过程中的作用.
研究的目的:
- 识别和描述一种新的调节途径,涉及H. pylori诱导的胃癌.
- 阐明MSTRG.10627.1/miR-142-5p/ADAMTS5轴在GC细胞行为中的功能.
- 在体内验证ADAMTS5在GC进展和转移中的作用.
主要方法:
- RNA测序和生物信息学分析以选lncRNA-miRNA-mRNA调节通路.
- 双 luciferase 记者测定以确认路径组件之间的相互作用.
- 在体外测试 (克隆原性形成,细胞迁移) 和西部涂抹以评估ADAMTS5功能和蛋白质表达.
- 使用裸体小鼠 (皮下和尾静脉注射) 的体内研究来评估瘤生长和转移.
主要成果:
- 一个重要的监管轴,MSTRG.10627.1-miR-142-5p-ADAMTS5,被确定并验证.
- 杆菌降低了GC细胞中ADAMTS5表达的调节 (p <0.05).
- 下调ADAMTS5增强了GC细胞的增殖,迁移和入侵,而ADAMTS5的过度表达抑制了这些过程 (p <0.05).
- 沉默ADAMTS5会增加PI3K和酸化AKT,并降低p53的表达,促进瘤生长和体内转移.
结论:
- 杆菌通过MSTRG.10627.1-miR-142-5p-ADAMTS5通路降低ADAMTS5的调节,有助于GC的发展.
- 观察到的PI3K,p-AKT和p53信号下游ADAMTS5的变化对H. pylori诱导的GC至关重要.
- 准ADAMTS5通路为H. pylori相关的胃癌提供了潜在的治疗策略.
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