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综合转录基因分析和实验验证确定ACADL是通过肺腺癌中的FOXO3a/PUMA轴作为线粒体瘤抑制剂

Ying Wang¹, Yan Ding²

¹Department of Respiratory and Critical Care Medicine, First Affiliated Hospital of Gannan Medical University, No. 23, Qingnian Road, Ganzhou, 341000, Jiangxi, China.

European journal of medical research

|January 6, 2026

概括

长链甲基CoA脱酶 (ACADL) 在肺腺癌 (LUAD) 中起到瘤抑制作用. 它通过激活FOXO3a/PUMA通路来抑制LUAD的进展,提供了一个潜在的治疗标.

科学领域:

在瘤学瘤学.
线粒体生物学线粒体生物学
癌症的分子机制

背景情况:

线粒体功能障碍是已知的癌症的标志.
肺腺癌 (LUAD) 中线粒体功能障碍的特定分子驱动因素尚未完全理解.

研究的目的:

为了确定参与LUAD病变的关键基因.
阐明长链乙-CoA脱酶 (ACADL) 在LUAD进展中的作用.
调查潜在的分子机制,包括FOXO3a/PUMA信号轴.

主要方法:

对含有线粒体相关基因的LUAD基因表达数据集 (GSE7670,GSE10072,GSE32863) 的综合分析.
使用LASSO回归和SVM-RFE算法识别枢纽基因.
在过度表达ACADL的LUAD细胞系和异种移植模型中的功能研究,包括对线粒体生物能学和信号通路激活的评估.

主要成果:

包括ACADL在内的8个枢纽基因显示,LUAD的诊断准确度很高.
过度表达ACADL抑制了LUAD细胞的增殖,迁移和入侵,同时诱导了亡.
ACADL通过改变ATP水平,活性氧物种 (ROS) 和线粒体动力学 (Drp1,Fis1,Mfn2) 来损害线粒体功能.
ACADL激活了FOXO3a/PUMA信号通路,在体内抑制了瘤的生长.

结论:

在LUAD中,ACADL作为线粒体相关瘤抑制剂起作用.
通过FOXO3a/PUMA信号通路,ACADL阻碍了LUAD的进展.
ACADL代表了对LUAD治疗的潜在治疗标.

关键词:

在 ACADL 和 ACADL 之间.在FOXO3a/PUMA路径中.肺部腺癌瘤是肺部腺癌.线粒体中的线粒体.

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