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外体miR-155-5p通过NF-κB激活调节乳腺癌的扩散和转移

Rui Xu¹, Chen-Xu Guo¹, Jun Qian¹

¹Department of Surgical Oncology, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.

Journal of biochemical and molecular toxicology

|November 3, 2025

概括

这项研究表明,高的miR-155-5p通过抑制NDFIP1和激活NF-κB通路来驱动乳腺癌 (BC) 的进展. 针对这种途径为新的BC诊断和治疗提供了潜力.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

乳腺癌 (BC) 仍然是女性癌症死亡的主要原因.
新的治疗策略对于改善BC患者的治疗结果至关重要.
微RNAs (miRNAs) 越来越多地被认为是它们在癌症发展中的作用.

研究的目的:

研究miR-155-5p在乳腺癌进展中的致癌作用.
为了阐明 miR-155-5p 驱动的 BC 背后的分子机制.
评估miR-155-5p作为潜在的诊断标记物和治疗点.

主要方法:

多omics方法包括血清外体和瘤组织的分析.
在体外功能测定 (增殖,运动,亡,入侵).
使用异种移植模型和基因淘汰/沉默的体内研究.

主要成果:

miR-155-5p在BC组织和血清外体中显著上调,与晚期和不良预后相关.
miR-155-5p促进了BC细胞的增殖,迁移,入侵,并抑制了细胞亡.
从机制上讲,miR-155-5p抑制了NDFIP1,激活了NF-κB通路 (p65转位,IL-6/TNF-α分泌).
在体内,miR-155-5p knockdown抑制了瘤生长和转移,NDFIP1沉默反转了效应.

结论:

在乳腺癌中,miR-155-5p/NDFIP1/NF-κB轴是关键的瘤性途径.
miR-155-5p是一个有前途的诊断生物标志物和BC的治疗目标.
综合性omics方法对于发现癌症调节网络是有价值的.
基于miRNA的干预措施显示出BC治疗的潜力.

关键词:

Nedd4 家庭相互作用蛋白 1 1 核因子-kappa B信号通路核因子-kappa B信号通路乳腺癌乳腺癌乳腺癌在 miR-155-5p 中, miR为155-5p.进行多主题分析.

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