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NR4A3通过调节PI3K/AKT/mTOR通路的自来抑制膀癌的进展

Li Fan¹, Feng Xu¹, Shouyong Liu¹

¹Department of Urology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu.

European journal of histochemistry : EJH

|June 30, 2025

概括

核受体NR4A3通过促进自抑制膀癌 (BC) 的进展. 针对NR4A3介导的自可能为膀癌患者提供新的治疗策略.

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:

膀癌 (BC) 是具有高复发率的侵袭性癌症.
自在癌症中具有双重作用,可能抑制或促进瘤生长.
抑制瘤的核受体NR4A3在BC中的作用仍然未被探索.

研究的目的:

研究NR4A3在膀癌进展中的作用.
阐明NR4A3在BC中的功能背后的机制,特别是它与自和PI3K/AKT/mTOR通路的关系.

主要方法:

在BC组织中进行NR4A3表达分析 (TCGA,免疫组织化学,RT-qPCR).
在BC细胞系 (5637,T24) 中使用lentiviral载体过度表达NR4A3.
评估细胞活力,增殖,迁移,入侵和细胞亡.
测量自标志物 (LC3,ATG5,贝克林-1,p62) 和PI3K/AKT/mTOR通路活性.

主要成果:

在BC组织中,NR4A3显著下调.
过度表达NR4A3抑制了BC细胞的增殖,迁移和入侵,并促进了细胞亡.
NR4A3增强了自标志物和抑制了PI3K/AKT/mTOR信号传递.
自的抑制逆转了NR4A3.3的抗瘤作用.

结论:

在膀癌中,NR4A3充当瘤抑制剂.
通过通过PI3K/AKT/mTOR途径促进自,NR4A3抑制了BC的进展.
通过NR4A3介导的自代表了膀癌的潜在治疗标.

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