LncRNA SNHG5 regulates the cell viability and apoptosis of glioma cells by the miR-1297/KPNA2 axis

Long non-coding RNA small nucleolar RNA host gene 5 (lncRNA SNHG5) has been reported to participate in the occurrence and development of glioma. However, the function and underlying molecular mechanisms of SNHG5 in glioma remain largely unknown. The expressions of SNHG5, microRNA-1297 (miR-1297) and karyopherin subunit alpha 2 (KPNA2) in glioma tissues and cells were evaluated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) or western blot. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry were used to detect cell viability and apoptosis, respectively. Western blot was also performed to detect the expressions of autophagy-associated proteins. The relationship among lncRNA SNHG5, miR-1297 and KPNA2 was verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. SNHG5 and KPNA2 were over expressed, and the level of miR-1297 was down-regulated in glioma tissues and cell lines. Knockdown of SHNG5 promoted apoptosis, while suppressing cell viability and autophagy of A172 and LN340 cells. Meanwhile, SHNG5 harbored the binding sites with miR-1297, and a negative correlation between the expression of SNHG5 and miR-1297 in glioma tissues was also observed. Interestingly, silencing of miR-1297 undermined the SHNG5 depletion-mediated effect on cell viability, apoptosis, and autophagy. KPNA2 was a direct target of miR-1297, and negatively regulated by miR-1297. More importantly, gain of KPNA2 mitigated the effect of SHNG5l knockdown on glioma cells. Silencing of SNHG5 had an implication in inhibiting apoptosis and stimulating cell viability and autophagy by the miR-1297/KPNA2 axis in glioma.