Abstract
Malignant glioma is the most frequent primary brain tumor in adults. Accumulated evidence showed that long non-coding RNA (lncRNA) long intergenic noncoding RNA 152 (LINC00152) participated in the progression of glioma, while the regulatory mechanisms remain elusive. Here, the study aimed to clarify the partial molecular mechanism of the lncRNA RNA component of mitochondrial RNA processing endoribonuclease (LINC00152) in the progression of glioma. The level of LINC00152, microRNA-613 (miR-613) and the cluster of differentiation 164 (CD164) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) in glioma tissues and cell lines. Western blot was used to detect the expression of CD164, phosphatidylinositol 3' -kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (AKT), phosphorylated AKT (p-AKT), matrix metalloproteinase 9 (MMP9), BCL2-Associated X (Bax) and c-Myc. Moreover, flow cytometry was carried out to identify cell apoptosis in vitro. Cell migration and invasion in T98G and LN18 cells were determined via transwell assay. Cell proliferation was analyzed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Meanwhile, dual-luciferase reporter and RNA immunoprecipitation (RIP) assay were performed to examine the interrelation between miR-613 and LINC00152 or CD164. The levels of LINC00152 and CD164 were obviously increased while miR-613 was especially decreased in glioma tissues and cell lines. The downregulation of LINC00152 and CD164, as well as the upregulation of miR-613 induced cell apoptosis, repressed viability, migration, and invasion. Furthermore, miR-613 was a target gene of LINC00152, while targeted CD164. The knockdown of LINC00152 promoted the expression of Bax, suppressed the levels of PI3K, p-PI3K, AKT, p-AKT, c-Myc, and MMP9. Interestingly, the downregulation of miR-613 or upregulation of CD164 restored the effect of low-expression of LINC00152 on cell proliferation, apoptosis, migration, invasion and the expression of relative proteins in vitro. Low-expression of LINC00152 modified cell proliferation, apoptosis migration and invasion through LINC00152/miR-613/CD164 axis via PI3K/AKT signaling pathway in glioma, thus providing new therapeutic target in the clinical treatment of glioma.