In recent years, the mortality rate of lung adenocarcinoma (LUAD) is persistently increasing, which has already caused a huge impact on human living standards. Hence, there is an urgent need to probe the molecular mechanism of LUAD progression, so as to disclose prognostic and diagnostic markers for patients with LUAD. Methylation 450 K data and mRNA expression data of LUAD were obtained via bioinformatics analysis to screen methylation-driven genes. The expression of the target gene was detected through qRT-PCR, while the methylation level was evaluated via methylation-specific PCR (MSP). The impact of the gene on cell proliferation, migration, invasion, apoptosis and cell cycle was measured through CCK-8, wound healing, Transwell invasion assay, and flow cytometry. CFTR was defined by bioinformatics analysis as the target gene for this study. qRT-PCR revealed that CFTR was lowly expressed in LUAD cells. MSP displayed that the CFTR promoter region in LUAD cells was hypermethylated, and demethylation could pronouncedly increase the level of CFTR mRNA in LUAD cells. Cell biological functional experiments exhibited that CFTR hindered cell proliferation, migration, and invasion, fostered cell apoptosis of LUAD, and blocked the cell cycle in G2-M phase. CFTR was hypermethylated in LUAD, which mediated the low expression of CFTR in LUAD to stimulate the progression of LUAD.

近年来，肺腺癌（LUAD）的死亡率持续上升，已对人类生活水平造成巨大影响。因此，迫切需要探索LUAD进展的分子机制，以揭示LUAD患者的预后和诊断标志物。通过生物信息学分析获得LUAD的甲基化450 K数据和mRNA表达数据，以筛选甲基化驱动基因。通过qRT-PCR检测靶基因的表达，而通过甲基化特异性PCR（MSP）评估甲基化水平。通过CCK-8、伤口愈合、Transwell侵袭试验和流式细胞术测量该基因对细胞增殖、迁移、侵袭、凋亡和细胞周期的影响。CFTR通过生物信息学分析被定义为本研究的靶基因。qRT-PCR 显示 CFTR 在 LUAD 细胞中低表达。MSP显示LUAD细胞CFTR启动子区域高度甲基化，去甲基化可显着增加LUAD细胞CFTR mRNA水平。细胞生物学功能实验表明，CFTR抑制细胞增殖、迁移和侵袭，促进LUAD细胞凋亡，阻断细胞周期G2-M期。CFTR在LUAD中被高甲基化，从而介导了LUAD中CFTR的低表达，从而刺激了LUAD的进展。和侵袭，促进 LUAD 细胞凋亡，阻断 G2-M 期细胞周期。CFTR在LUAD中被高甲基化，从而介导了LUAD中CFTR的低表达，从而刺激了LUAD的进展。和侵袭，促进 LUAD 细胞凋亡，阻断 G2-M 期细胞周期。CFTR在LUAD中被高甲基化，从而介导了LUAD中CFTR的低表达，从而刺激了LUAD的进展。