LncRNA ZFAS1/miR-1271-5p/HK2 Promotes Glioma Development Through Regulating Proliferation, Migration, Invasion and Apoptosis.

Abstract

Glioma is the common type of malignant tumor with high mortality worldwide. Survival rate of patients with glioma remains poor, and almost half of patients died within 15 months. The increasing researches indicated that long non-coding RNA (lncRNA) Zinc finger antisense 1 (ZFAS1) played essential roles in tumor initiation and progression. Therefore, it is worth clarifying potential role of ZFAS1 in glioma. The expression levels of ZFAS1, miR-1271-5p, and Hexokinase 2 (HK2) in glioma tissues and cells were examined by real-time quantitative polymerase chain reaction (RT-qPCR). Kaplan-Meier curve was employed to analyze the relationship between cumulative survival time of glioma patients and expression level of ZFAS1. The cell proliferation, apoptosis, and mobility ability were assessed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), flow cytometry, and transwell assays. The relationship among ZFAS1, miR-1271-5p, and HK2 was analyzed by bioinformatics assay, dual-luciferase reporter and Pearson's correlation analyses. The protein expression level of HK2 was examined by western blot assay. Finally, a xenograft experiment was established to assess the effects of ZFAS1 silencing in vivo. ZFAS1 was highly expressed in glioma tissues and cells, besides, the expression level of ZFAS1 was associated with survival time of glioma patients. Functional experiments suggested that knockdown of ZFAS1 or upregulation of miR-1271-5p constrained proliferation, migration and induced apoptosis of glioma cells. In addition, miR-1271-5p, interacted with HK2, was a target of ZFAS1. The gain of HK2 could overturn ZFAS1 silencing-induced effects on glioma cells. Besides, deficiency of ZFAS1 hindered tumor growth in vivo. ZFAS1 was involved in proliferation, migration, and apoptosis of glioma cells via regulating miR-1271-5p/HK2 axis.