MicroRNA‑92a promotes non‑small cell lung cancer cell growth by targeting tumor suppressor gene FBXW7.

MicroRNA (miRNA/miR)‑92a has been identified as being significantly downregulated in non‑small cell lung cancer (NSCLC) tissues using a miRNA array. However, its biological function and molecular mechanisms in NSCLC have not been fully elucidated. The aim of the present study was to determine the role of miR‑92a in NSCLC and the mechanisms by which it affects NSCLC cells. The expression levels of miR‑92a in NSCLC tissues and cell lines were analyzed using reverse transcription‑quantitative PCR. Cell viability and cell apoptosis were determined using an MTT assay and flow cytometry, respectively. It was observed that miR‑92a was significantly upregulated in NSCLC tissues and cell lines. Inhibition of miR‑92a significantly suppressed viability of NSCLC cells, with concomitant downregulation of key proliferative genes, such as proliferating cell nuclear antigen and Ki‑67. miR‑92a downregulation induced apoptosis of NSCLC cells, as evidenced by flow cytometry and apoptosis‑related protein detection. Luciferase assays confirmed that miR‑92a could directly bind to the 3'‑untranslated region of tumor suppressor F‑box/WD repeat‑containing protein 7 (FBXW7) and suppress its translation. Furthermore, small interfering RNA‑mediated FBXW7 inhibition partially attenuated the tumor suppressive effect of an miR‑92a inhibitor on NSCLC cells. Collectively, these findings demonstrated that miR‑92a might function as an oncogene in NSCLC by regulating FBXW7. In conclusion, miR‑92a could serve as a potential therapeutic target in NSCLC treatment.