Suggest that miRNA-124 may regulate non-small cell lung carcinoma cell proliferation via decreasing SOX8.

our findings suggest that miR-124 functions as a tumor suppressor by targeting STAT3, and that miR-124 may potentially serve as a useful biomarker for the prognosis of non-small cell lung cancer patients.

data show a novel feedback loop between miR-124 and transforming growth factor-beta (TGF-beta) pathway driving non-small cell lung cancer (NSCLC) metastasis, which might provide a new insight into treatment of NSCLC progression

miR-124 functions as a tumor suppressor in lung adenocarcinoma by directly targeting SOX9.

miR-124 inhibits lung cancer cell migration and invasion through suppressing epithelial-mesenchymal transition (EMT) and inducing apoptosis of the lung cancer cells.

miR-124 plays a new critical role in acquired resistance to gefitinib in non-small cell lung cancer. miR-124 decreased SNAI2 and STAT3 expression by directly targeting their 3'UTRs.

AKT inhibition blocks miR-124 silencing-induced AKT1/2, glucose transporter 1, hexokinase II activation, cell proliferation, and glycolytic or energy metabolism changes. In summary, this study demonstrated that miR-124 is able to inhibit proliferation, glycolysis, and energy metabolism, potentially by targeting AKT1/2-glucose transporter 1/hexokinase II in non-small cell lung cancer cells.

circHIPK3 promotes lung cancer cell progression possibly by sponging miR-124.

MiR-124 changes the sensitivity of lung cancer cells to cisplatin through targeting STAT3.

Decreased miR-124 contributes to the epithelial-mesenchymal transition phenotype formation of lung adenocarcinoma cells via targeting enhancer of zeste homolog 2.