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

Abstract

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.