Suppression of miR-221 inhibits glioma cells proliferation and invasion via targeting SEMA3B

• Published in: Biological research Vol. 48; no. 1; p. 37
• Main Authors: Cai, Guilan, Qiao, Shanshan, Chen, Kui
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 22.07.2015; BioMed Central; Sociedad de Biología de Chile; BMC
• Subjects: Analysis; Apoptosis; BIOLOGY; Blotting, Western; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Cancer metastasis; Cell Line, Tumor; Cell Movement; Cell Proliferation; Gene Expression Regulation, Neoplastic; Glioma; Glioma - metabolism; Glioma - pathology; Gliomas; Humans; Luciferases - metabolism; Membrane Glycoproteins - genetics; Membrane Glycoproteins - pharmacology; MicroRNAs - antagonists & inhibitors; MicroRNAs - metabolism; miR-221; Neoplasm Invasiveness; Real-Time Polymerase Chain Reaction; SEMA3B; Semaphorins - genetics; Semaphorins - pharmacology; Signal Transduction; Cancer metastasis; Glioma; miR-221; SEMA3B
• ISSN: 0717-6287; 0716-9760; 0717-6287
• DOI: 10.1186/s40659-015-0030-y

Gliomas are the most common primary tumors in the central nervous system. Due to complicated signaling pathways involved in glioma progression, effective targets for treatment and biomarkers for prognosis prediction are still scant. In this study we revealed that a new microRNA (miR), the miR-221, was highly expressed in the glioma cells, and suppression of miR-221 resulted in decreased cellular proliferation, migration, and invasion in glioma cells. Mechanistic experiments validated that miR-221 participates in regulating glioma cells proliferation and invasion via suppression of a direct target gene, the Semaphorin 3B (SEMA3B). The rescue experiment with miR-221 and SEMA3B both knockdown results in significant reversion of miR-221 induced phenotypes. Taken together, our findings highlight an unappreciated role for miR-221 and SEMA3B in glioma.