SNHG7 Facilitates Glioblastoma Progression by Functioning as a Molecular Sponge for MicroRNA-449b-5p and Thereby Increasing MYCN Expression

BACKGROUND AND AIMS: Long noncoding RNA (small nucleolar RNA host gene 7) has been reported to be involved in multiple malignancies and acts as an oncogene. However, the potential mechanism of small nucleolar RNA host gene 7 in glioblastoma is rarely known. In this study, we attempted to elucidate the biological effects of small nucleolar RNA host gene 7 and the possible molecular mechanism in glioblastoma. METHODS: The expression level of small nucleolar RNA host gene 7 in glioblastoma tissues and corresponding tumor cell lines was evaluated by using quantitative real-time polymerase chain reaction. Bioinformatics analyses and dual-luciferase reporter gene assay were conducted to verify the correlation among small nucleolar RNA host gene 7, miR-449b-5p, and MYCN. The role of small nucleolar RNA host gene 7 on cell viability, migration, and invasion was measured. RESULTS: Small nucleolar RNA host gene 7 expression was markedly increased in glioblastoma tumor tissue. Small nucleolar RNA host gene 7 can sponge miR-449b-5p and negatively regulate miR-449b-5p expression. MiR-449b-5p was remarkably repressed in glioblastoma tissues. Reduction of miR-449b-5p reversed the repressive effects of small nucleolar RNA host gene 7 knockdown on cellular behaviors in glioblastoma. In addition, miR-449b-5p can directly bind with MYCN. Compared with normal samples, MYCN expression was increased. The MYCN expression was negatively related to miR-449b-5p expression while positively related to small nucleolar RNA host gene 7 expression. Rescue experiments revealed that MYCN overexpression reversed the repressive role of small nucleolar RNA host gene 7 knockdown on viability, migration, and invasion of U251 cells. CONCLUSION: In summary, our results demonstrated that small nucleolar RNA host gene 7 regulates glioblastoma proliferation, migration, and invasion via regulating miR-449b-5p and its target gene MYCN, thereby providing a potential therapeutic target for glioblastoma.