通过FUCA2/GGH信号传导对细胞周期和上皮-间质转化的调控促进了肺腺癌的进展。
The regulation of the cell cycle and epithelial-mesenchymal transition through FUCA2/GGH signaling promotes the progression of lung adenocarcinoma.
作者信息
Peng Yuanyuan, Yang Xingyu, Liu Yafeng, Zhou Jiawei, Guo Jianqiang, Ma Bingfeng, Bai Ying, Wu Jing, Hu Dong
机构信息
Department of Immunology, School of Medicine, Anhui University of Science and Technology, Huainan City, China; Anhui Province Engineering Laboratory of Occupational Health and Safety, School of Medicine, Anhui University of Science and Technology, Huainan City, China.
Department of Immunology, School of Medicine, Anhui University of Science and Technology, Huainan City, China; Anhui Province Engineering Laboratory of Occupational Health and Safety, School of Medicine, Anhui University of Science and Technology, Huainan City, China; Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, School of Medicine, Anhui University of Science and Technology, Huainan City, China.
出版信息
Gene. 2025 Mar 5;939:149183. doi: 10.1016/j.gene.2024.149183. Epub 2024 Dec 20.
The development of lung adenocarcinoma (LUAD) is intricately linked with cell cycle regulation and epithelial-mesenchymal transition (EMT). Our study, leveraging bioinformatics and database analysis, identified FUCA2 as a key gene influencing the prognosis and progression of LUAD. We observed that FUCA2 is highly expressed in LUAD and correlates with poor outcomes. Functionally, we assessed the role of this gene through cell cloning, scratch assays, transwell migration, and western blotting, revealing that FUCA2 knockdown significantly inhibits tumor cell proliferation and migration, downregulates the expression of cell cycle and EMT-related proteins, and markedly reduces tumor burden. Mechanistically, pathway enrichment analysis identified GGH as a downstream target of FUCA2. Knockdown of GGH similarly inhibits the proliferation, migration, and cell cycle progression of LUAD cells. FUCA2 upregulates GGH to modulate cell cycle and EMT in LUAD. Collectively, our findings indicate that the FUCA2/GGH axis promotes LUAD progression by regulating cell cycle and EMT.
肺腺癌（LUAD）的发展与细胞周期调控和上皮-间质转化（EMT）密切相关。我们的研究利用生物信息学和数据库分析，确定FUCA2是影响LUAD预后和进展的关键基因。我们观察到FUCA2在LUAD中高表达，且与不良预后相关。在功能上，我们通过细胞克隆、划痕试验、Transwell迁移和蛋白质免疫印迹评估了该基因的作用，结果显示FUCA2基因敲低显著抑制肿瘤细胞增殖和迁移，下调细胞周期和EMT相关蛋白的表达，并显著减轻肿瘤负担。从机制上讲，通路富集分析确定GGH是FUCA2的下游靶点。敲低GGH同样会抑制LUAD细胞的增殖、迁移和细胞周期进程。FUCA2上调GGH以调节LUAD中的细胞周期和EMT。总的来说，我们的研究结果表明，FUCA2/GGH轴通过调节细胞周期和EMT促进LUAD进展。
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