Abstract
Glioma is a common malignant human brain tumor. The progression of glioma is associated with dysregulation of various microRNAs. Previous studies have demonstrated that microRNA-26b-3p (miR-26b-3p) is correlated with the pathogenesis of various tumors, but the functional role of miR-26b-3p and its underlying mechanisms in glioma are not clear. Here, we found that overexpression of miR-26b-3p repressed cell migration and proliferation and promoted apoptosis. In contrast, the opposite effects were observed when miR-26b-3p was inhibited in glioma cells. Anthrax toxin receptor 1 (ANTXR1) was confirmed to be a downstream molecule of miR-26b-3p. Reintroduction of ANTXR1 with an ORF region rescued the suppressive effects of miR-26b-3p on proliferation and migration, and inhibited the apoptosis of glioma cells. Moreover, the downstream target of miR-26b-3p, ANTXR1, was increased in glioma tissues and was inversely correlated with miR-26b-3p. MiR-26b-3p and ANTXR1 were correlated with the severity of glioma. Taken together, these results demonstrate that miR-26b-3p is a critical modulator of glioma via its downstream molecule, ANTXR1. Further, the miR-26b-3p/ANTXR1 axis may serve as a treatment or diagnostic target in glioma.