Study on the Effects of miR-490-3p on the Malignant Biological Behavior of Lung Tumor Cell A549 and Its Molecular Mechanism

The objective of this research was to prove whether miR-490-3p regulated the propagation, migration, and invasion of lung tumor cells using targeting sequence similarity as family 83F (FAM83F). The gene expression of miR-490-3p and FAM83F of human embryonic lung fibroblasts (HELF) and lung cancer cells (A549, H1299, 95D) were analyzed using real-time quantitative reverse transcription-polymerase chain reaction PCR (RT-qPCR) and western blot. Analysis of the targeted relationship of miR-490-3P with FAM83F was performed through double luciferase reporting assays with the addition of western blotting. The impacts of miR-490-3p and FAM83F gene expression were tested by cell counting kits (CCK-8), a scraping healing test, and a transwell test on the proliferation activity, scratch healing rate, and the numbers of migrating and invading A549 cells. Impacts of miR-490-3P and FAM83F expressions on the phosphorylated protein kinase B' (p-AKT) expression were tested with western blotting. miR-490-3P gene expressions in A549 were observably less expressed compared to that of HELF cells, but the mRNA and protein expressions of FAM83F were observably greater than those in HELF (P < 0.05), which indicates that miR-490-3p-bound FAM83F regulates the expression of FAM83F immediately and negatively. After up-regulating miR-490-3p expression or down-regulating FAM83F expression, the proliferation activity, rate of wound-healing, the numbers of migrating and invading cells, and p-AKT protein expression of A549 cells were observably reduced (P < 0.05). Compared to upregulation of miR-490-3p, the propagation activity, wound-healing rate, numbers of migrating and invading cells, and expression of the P-Akt protein of A549 cells were significantly decreased after the upregulation of miR-490-3p and FAM83F (P < 0.05). MiR-490-3p observably inhibited migration and invasion in lung cancer cells with negatively regulating expression of FAM83F, and the mechanisms might be relevant to restraining the AKT pathway.