LncRNA SNHG16 Promotes Proliferation, Migration, and Invasion of Glioma Cells Through Regulating the miR-490/PCBP2 Axis

Background: Glioma is the most common tumor of the central nervous system, which has a high mortality and recurrence rate. Increasing evidence shows that long noncoding RNAs (lncRNA) are closely related to the occurrence of cancer. However, the mechanism of lncRNA small nucleolar RNA host gene 16 (SNHG16) in glioma remains to be studied. Materials and Methods: The expression levels of SNHG16, microRNA-490 (miR-490), and poly(C)-binding proteins 2 (PCBP2) in tissues and cells were determined by quantitative real-time polymerase chain reaction. 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and transwell assays were used to evaluate the proliferation, migration, and invasion abilities of glioma cells. Moreover, Western blot analysis was performed to assess the levels of PCBP2 and proliferation-related and metastasis-related proteins. Dual-luciferase reporter assay was used to verify the interaction among SNHG16, miR-490, and PCBP2. Results: SNHG16 was highly expressed in glioma tissues and cells, and silenced-SNHG16 suppressed the proliferation, migration, and invasion of glioma cells. Besides, SNHG16 could interact with miR-490. The aberrant expression of SNHG16 restored the inhibitory effect of miR-490 overexpression on the proliferation, migration, and invasion of glioma cells. Moreover, PCBP2 was a target of miR-490. MiR-490 inhibitor recovered the suppression effect of PCBP2 knockdown on glioma progression, and PCBP2 overexpression also could reverse the inhibition effect of miR-490 mimic on glioma progression. In addition, SNHG16 promoted the expression of PCBP2, while miR-490 inhibited its expression. Conclusions: The authors' data revealed that SNHG16 might function as an oncogene in glioma through regulating the miR-490/PCBP2 axis, and the elucidating of the mechanism of SNHG16 provided a potential therapeutic target for glioma.