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Background: Long intergenic non-protein coding RNA 1426 (LINC01426) is up-regulated in glioma and functions as a tumor promoter. However, the role of LINC01426 in glioma required further exploration. Therefore, this article mainly studied the role and possible mechanism of LINC01426 in glioma. Methods: The area under the receiver operating characteristic curve was used to determine the diagnostic value of LINC01426. The effect of LINC01426 on tumor growth was analyzed by tumorigenesis assay and immunohistochemical analysis. Bioinformatics analysis, dual-luciferase assay, RNA pull-down, Pearson test, and real-time quantitative PCR (RT-qPCR) were applied to verify the relationship between target genes. The expressions and effects of LINC01426, miR-661 and MDM2 proto-oncogene (Mdm2) in glioma were examined by bioinformatics analysis combined with molecular and functional experiments (RT-qRCR, 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide, clone formation, BrdU, flow cytometry). The expressions of proliferation and apoptosis-related proteins were determined by Western blot. Results: LINC01426, which was high-expressed in glioma and was related to poor prognosis, could be used as a diagnostic marker for glioma. SiLINC01426 inhibited the malignant phenotype of glioma cells in vitro and attenuated tumor growth and PCNA expression in vivo, while the effects of LINC01426 were the opposite. LINC01426 targeted and inversely correlated with miR-661, which was low-expressed in glioma. MiR-661 inhibitor evidently overturned the effect of siLINC01426 on biological functions, proliferation, and apoptosis-related proteins of glioma cells. Mdm2 bound to miR-661. Moreover, siMdm2 reversed the effects of miR-661 inhibitor on the biological characteristics and Mdm2/p53/p21 expression of glioma cells. Conclusion: LINC01426 aggravated the malignant progression of glioma through miR-661/Mdm2 axis. |
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