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

Abstract

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.