miRNA‑1271 inhibits cell proliferation in neuroglioma by targeting fibronectin 1.

miR-1271 is a multifunctional post-translational modulator, which is involved in several diseases. However, the association between microRNA (miR)‑1271 and fibronectin 1 (FN1) remains to be fully elucidated in neuroglioma. In the present study, it was hypothesized that a post‑translational mechanism of miR‑1271 regulates the expression of FN1 in the progression of neuroglioma. The present study aimed to investigate the clinical significance and underlying molecular mechanisms of miRNA‑1271 in the development of glioma. The miR‑1271 levels in glioma tissues and cell lines were assessed using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). miR‑1271 mimics and inhibitors were transfected to gain or loss of miR‑1271 function. Cell proliferation was analyzed by using an MTT assay. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. The mRNA and protein levels were assessed by RT‑qPCR and western blotting. The results showed that miR‑1271 was downregulated in glioma tumor tissues and cell lines. In addition, it was demonstrated that low levels of miR‑1271 in patients with glioma were correlated with low survival rate. In vitro, the cell viability was significantly suppressed following transfection with miRNA‑1271 mimics and increased following transfection with the miRNA‑1271 inhibitor. The miRNA‑1271 mimics induced cell apoptosis and the miRNA‑1271 inhibitor suppressed cell apoptosis in H4 and U251 cell lines. Furthermore, the 3'‑untranslated region of FN1 was bound by miR‑1271. Therefore, it was concluded that miR‑1271 inhibited glioma cell growth by targeting FN1, and a low level of miR‑1271 in glioma tumor tissues was associated with lower survival rates in patients with glioma.