The expression of microRNA 21 (miR-21) has been reported to be upregulated in various types of cancer, including malignant gliomas. However, its functions and mechanisms in glioma remain to be fully elucidated. The present study established miRNA-21 overexpression and knockdown cell lines using SRY-box 2 (Sox2) small interfering RNA (siRNA) to knockdown expression and Sox2 cDNA was cloned into pcDNA 3.1 mammalian expression vector for ectopic expression. BIO and XAV-939 were used for β-catenin signaling activation and knockdown, respectively. Transwell chambers were used to assay the capacity of cells to migrate. The present study determined that increased expression of miR-21 significantly promoted the migration and invasion of glioma cells, which was accompanied by an upregulated expression of the Sox2 protein. Sox2 overexpression also promoted glioma cell migration and invasion, whereas Sox2 siRNA markedly reduced the miR-21-enhanced migration and invasion of glioma cells, indicating Sox2 may act as a crucial mediator of miR-21 function. Furthermore, miR-21 also upregulated the protein expression level of β-catenin, whereas anti-miR-21 and Sox2 knockdown significantly reduced β-catenin expression. BIO, a β-catenin specific agonist, enhanced migration and invasion of glioma cells. XAV-939, an inhibitor of β-catenin signaling, markedly inhibited the migration and invasion of glioma cells, suggesting that β-catenin may be associated with miR-21- and Sox2-induced invasion of glioma cells. Notably, BIO restored the migration and invasion potential of glioma cells, which were inhibited by Sox2 siRNA and anti-miR-21. These findings indicated that β-catenin may be an important downstream mediator of miR-21 and Sox2. Therefore, the present study identified the miR-21/Sox2/β-catenin signaling pathway, which may regulate the migration and invasion of human glioma cells.

Due to its high invasiveness, glioblastoma is difficult to treat by surgery, radiotherapy, chemotherapy or any combination therapy. Syndecan binding protein (SDCBP), a widely distributed intracellular scaffold protein, has an important role in both physiological and pathological process. In the current work, we have identified target sequences for miR-135a-5p and miR-124-3p in the 3'-untranslated region of the SDCBP mRNA. Therefore, we have investigated the relationship between SDCBP, miR-135a-5p and miR-124-3p in glioblastoma multiforme cells T98G and U87 in vitro and in vivo. Dual luciferase activity assay documented that SDCBP is, in fact, the target of miR-135a-5p, miR-124-3. Western blot, qRT-PCR, proliferation, migration, and invasion assays have demonstrated that of silencing SDCBP or overexpressing miR-135a-5p/miR-124-3p significantly interferes with the malignant properties of glioblastoma cells. In vivo studies have shown that silencing SDCBP or overexpressing miR-135a-5p/miR-124-3p result in a marked decrease of tumor size and prolong life of tumor-bearing mice. A therapy combining the three treatments inhibits synergistically subcutaneous tumor growth in nude mice. In conclusion, proliferation, migration and invasion of glioblastoma can be inhibited by targeted regulation of SDCBP through upregulation of miR-135a-5p and miR-124-3p.

Background Neurovascular contact (NVC) is the main cause of primary trigeminal neuralgia (PTN); however, cases of PTN without NVC are still observed. In this study, the Meckel cave (MC) morphology in PTN were analyzed by radiomics and compared to healthy controls (HCs) to explore the cause of PTN. Methods We studied the 3.0T MRI data of 115 patients with PTN and 46 HCs. Bilateral MC was modeled using the 3D Slicer software, and the morphological characteristics of MC were analyzed using the radiomics method. Results The right side incidence rate in the PTN group was higher than the left side incidence. By analyzing the flatness feature of MC, we observed that the affected side of the PTN was lower than that of the unaffected side, the right MC of the PTN and HC was lower than that of the left MC, the MC of the affected side of the left and right PTN without bilateral NVC was lower than that of the unaffected side. Conclusions By providing a method to analyze the morphology of the MC, we found that there is an asymmetry in the morphology of bilateral MC in the PTN and HC groups. It can be inferred that the flatness of the MC may be a cause of PTN.