Objective:To investigate the expression level of LINC01106 in glioma tissues and cell lines and explore the potential mechanism through which LINC01106 affect the proliferation and invasion of glioma cells. Methods:The expression level of LINC01106 in glioma tissues was analyzed by The Cancer Genome Atlas(TCGA)database. QRT-PCR was carried out to detect LINC01106 expression level in glioma tissues and cell lines. The small interfering RNA(siRNA)and overexpressed plasmid(OE)of LINC01106 were applied to suppress or increase the expression level of LINC01106 in U87 cell lines,respectively. CCK-8 assay,EdU assay and transwell assay were performed to assess the effect of LINC01106 on the proliferative and invasive ability of U87 cells. Bioinformatics analysis and in vitro cell experiments were conducted to further explore the potential mechanism of LINC01106. Results:Analysis of the TCGA database revealed that the expression level of LINC01106 was remarkably decreased in glioma tissues. Besides,the results of qRT-PCR showed that the expression levels of LINC01106 in glioma tissues and cell lines were significant lower that in normal controls. Repression of LINC01106 in U87 cells markedly promoted the proliferative and invasive capacities of glioma cells,while overespression of LINC01106 exerted the opposite effects. Bioinformatics analysis and double luciferase reporter gene assay revealed that LINC01106 could bind to miR-3167 and inhibit its expression,while miR-3167 might target CBFA2T3,which might be a potential mechanism for the progression of LINC01106 in glioma. Conclusion:LINC01106 is down-regulated in glioma,and inhibition of LINC01106 can promote the proliferation and invasion of glioma cells. LINC01106 might play its role as a tumor suppressor in gliomas by competitively binding to CBFA2T3 with miR-3167.