Lung adenocarcinoma (LUAD) is typically featured by a low 5-year survival rate, hence there is a necessary to investigate new biomarkers in LUAD progression. Competing endogenous RNA (ceRNA) network has… Click to show full abstract
Lung adenocarcinoma (LUAD) is typically featured by a low 5-year survival rate, hence there is a necessary to investigate new biomarkers in LUAD progression. Competing endogenous RNA (ceRNA) network has been widely reported in the regulation of tumor processes, which is also the main direction of this paper. Based on the data of GEPIA database, lncRNA MAFG-AS1 was upregulated in LUAD tissues, which was associated with poor prognosis of patients. Proliferation or apoptosis of LUAD cells were measured by CCK-8, EdU and caspase-3 activity assays followed by Western blot. The results indicated that silencing of MAFG-AS1 suppressed cell proliferation but induced cell apoptosis. RNA FISH staining showing the cytoplasmic localization of MAFG-AS1 in LUAD cells. Mechanism detection revealed that MAFG-AS1 served as a molecular sponge of miR-744-5p to upregulate its nearby gene MAF bZIP transcription factor G (MAFG) in LUAD cells. Functionally, MAFG overexpression attenuated the cellular processes mediated by MAFG-AS1 knockdown. In summary, this study unveiled the MAFG-AS1/miR-744-5p/MAFG axis in LUAD, providing a potent and promising therapeutic target for LUAD patients.
               
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