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外体环0000549通过miR-15b-5p/KIF1B促进MNNG诱导的胃癌

Zhaofeng Liang¹, Zihan Gao¹, Yue Zhang²

¹Wujin Institute of Molecular Diagnostics and Precision Cancer Medicine of Jiangsu University, Wujin Hospital Affiliated with Jiangsu University, Changzhou, Jiangsu 213017, P.R. China.

International journal of molecular medicine

|March 6, 2026

概括

化物暴露通过外体促进胃癌 (GC). 外体环0000549通过调节miR-15b-5p/KIF1B/PI3K/AKT通路来驱动恶性转变,提供潜在的GC生物标志物.

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:

环境因素,特别是酸盐,与胃癌 (GC) 的发展有关.
外基因组在致癌过程中调解细胞间的通信.
甲基N-N' - 尼特罗-N-尼特罗斯瓜尼丁 (MNNG) 在GES-1细胞中诱导恶性转变,产生促进GC的外体.

研究的目的:

调查外体环RNAs在MNNG诱导的胃癌发生中的作用.
为了识别和验证参与GC进展的候选circRNAs.
阐明外部体促进GC启动和发展的机制.

主要方法:

使用MNNG暴露的GES-1细胞建立恶性转化模型.
生物信息学分析用于选和验证候选circRNAs.
功能性测试,包括细胞培养实验和裸体小鼠模型.
机械学研究以确定分子标和信号通路.

主要成果:

Circ0000549在暴露于MNNG的细胞,它们的外体和GC患者的血清外体中显著上调.
在GES-1细胞中,circ0000549的过度表达增强了恶性特征,上皮-介质细胞过渡和干细胞.
外体环0000549在体内促进了MNNG诱导的胃癌发生.
Circ0000549作为miR-15b-5p的海绵,增加KIF1B的表达,并激活PI3K/AKT通路.

结论:

外体环0000549通过miR-15b-5p/KIF1B/PI3K/AKT轴促进了GES-1细胞的恶性转化.
Circ0000549是MNNG诱导的胃癌发生的关键媒介.
外体环0000549显示出作为GC的诊断和预后生物标志物以及治疗点的潜力.

关键词:

周围的时间000054949 N-甲基-N' - 尼特罗-N-尼特罗斯古安尼丁.化学致癌发生是化学致癌.外基因组是外基因组中的一个.胃癌胃癌是一种胃癌.微型RNA 15b-5p 的情况.

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