2020 Volume 43 Issue 4 Pages 639-648
Sema3C has been reported to promote glioma stem cells self-renewal and glioblastoma growth. However, the prognostic value and the regulatory mechanism for its abnormal expression in glioma remain poorly understood. In the current study, the immunohistochemistry results demonstrated that Sema3C was overexpressed in 169 of 216 (78.2%) interpretable glioma patients compared with 3 of 15 (20.0%) interpretable non-neoplastic brain cases (p = 0.0001). Sema3C overexpression was significantly associated with histologic type (p = 0.008), high Ki67 labeling index (p = 0.02), tumor grade (p = 0.002) and wild type IDH1 (p = 0.0001). Importantly, its overexpression predicts the shorter overall survival of glioma patients (p = 0.0017), especially the ones with high grade (p = 0.0124). Functionally, Sema3C silencing significantly reduced the proliferation and invasion of glioma cells, indicating an oncogenic role of Sema3C in glioma in vitro. To elucidate the reason accounting for its overexpression, it is identified miR-142-5p as a tumor suppressor that directly targets Sema3C in glioma cells. miR-142-5p and Sema3C were co-regulators of epithelial–mesenchymal transition. Clinically, miR-142-5p expression was conversely related with Sema3C expression in glioma samples. Together, we identified that Sema3C could promote the progression of glioma and its expression was negatively regulated by miR-142-5p in vitro. Thus, the miR-142-5p-Sema3C axis plays importantly in glioma and holds potential to be therapeutic targets as well.