DNA Methylation-Mediated Low Expression of CFTR Stimulates the Progression of Lung Adenocarcinoma.

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.