miR-486-3p Suppresses Malignant Phenotypes and is Associated with Reduced WNT5B, DVL1, and β-catenin Expression in Lung Adenocarcinoma Cells.

Lung adenocarcinoma (LUAD) is the predominant histological subtype of non-small cell lung cancer and remains associated with substantial morbidity and mortality. Previous studies have identified tumor-suppressive functions of miR-486-3p in LUAD, but its relationship with WNT5B, DVL1, and β-catenin-related expression changes has not been clearly defined. Here, baseline miR-486-3p abundance was examined in A549 and H358 LUAD cells and compared with that in Beas-2b bronchial epithelial cells maintained under their respective routine conditions. Stable miR-486-3p-overexpressing models were generated by lentiviral transduction. Cell growth-associated activity, clonogenic growth, wound closure, and traversal of Matrigel-coated membranes were evaluated using Cell Counting Kit-8, colony-formation, wound-healing, and Transwell assays. WNT5B, DVL1, β-catenin, and BCL-2 protein abundance were assessed by Western blotting, and WNT5B, DVL1, CTNNB1, and BCL2 mRNA levels were additionally examined by RT-qPCR. Under the culture conditions used, miR-486-3p abundance was lower in A549 and H358 cells than in Beas-2b cells, and lentiviral transduction produced stable overexpression in both LUAD cell lines. Forced miR-486-3p overexpression reduced the CCK-8 signal, colony formation, wound closure, and Matrigel-coated membrane traversal and was accompanied by lower WNT5B, DVL1, total β-catenin, and BCL-2 protein abundance. RT-qPCR further showed lower WNT5B, DVL1, CTNNB1, and BCL2 transcript abundance in both LUAD cell lines after miR-486-3p overexpression. These findings support an in vitro association between forced miR-486-3p expression, attenuation of several malignant-cell readouts, and altered Wnt-related expression; however, they do not establish direct miRNA-target binding, pathway activity, or a causal linear signaling mechanism.