MicroRNA­4500 suppresses tumor progression in non­small cell lung cancer by regulating STAT3.

Research has revealed that microRNA (miR)­4500 is downregulated in non­small cell lung cancer (NSCLC), and miR­4500 suppresses tumor growth by targeting lin­28 homolog B and NRAS proto­oncogene, GTPase. In the present study, it was reported that signal transducer and activator of transcription 3 (STAT3) may function as a novel target gene for miR­4500 in NSCLC. The experiments conducted in the present study confirmed that the miR­4500 expression was decreased in NSCLC tissues and cells compared with adjacent normal tissues and a normal lung cell line. miR­4500 suppressed the cell proliferation, migration, invasion and promoted apoptosis of the human NSCLC cell lines A549 and H1975. Expression of STAT3 was negatively correlated with miR­4500 expression in vivo. A luciferase reporter assay suggested that miR­4500 directly targeted the 3' untranslated region of STAT3. The tumor inhibition effect of small interfering RNA STAT3 in A549 and H1975 lines may be partially impaired by a miR­4500 inhibitor. The results of the present study suggests that miR­4500 may be a tumor suppressor and a potential therapeutic target in NSCLC.

Upregulated microRNA­671­3p promotes tumor progression by suppressing forkhead box P2 expression in non­small­cell lung cancer.

In the present study, the expression of microRNA (miR)­671­3p in non­small­cell lung cancer (NSCLC) was detected via reverse transcription­quantitative polymerase chain reaction analysis, and its role in cell proliferation, apoptosis, migration and invasion was investigated via Cell Counting Kit­8, colony formation, flow cytometry, Transwell and scratch assays, respectively. It was observed that the expression of miR­671­3p was upregulated in NSCLC tissues and cell lines (A549 and H1975). Treatment with miR­671­3p inhibitors suppressed cell proliferation, migration and invasion, and increased apoptosis in vitro, suggesting that miR­671­3p functions as an oncogene in NSCLC. In addition, forkhead box P2 (FOXP2) has been reported to be a tumor suppressor that is downregulated in several types of cancer, and its low expression was confirmed in NSCLC tissues and cell lines in the current study via western blotting. The results of the luciferase reporter assay also demonstrated that miR­671­3p targeted directly the 3'­untranslated region of FOXP2. Furthermore, overexpression of FOXP2 in A549 and H1975 cell lines suppressed the growth, migration and invasion, and promoted apoptosis, whereas these effects were reversed by transfection with miR­671­3p mimics, suggesting that miR­671­3p promoted tumor progression via regulating FOXP2. Taken together, the results reported in the present study implied that miR­671­3p may be a potential therapeutic target in NSCLC.