Silencing lncRNA LINC01410 suppresses cell viability yet promotes apoptosis and sensitivity to temozolomide in glioblastoma cells by inactivating PTEN/AKT pathway via targeting miR-370-3p

Abstract

Background Long non-coding RNAs (LncRNAs) are involved in glioblastoma (GBM), but the role of long intergenic non-protein coding RNA 01410 (lncRNA LINC01410) is poorly understood. Methods The expression of LINC01410 in GBM tissues and cells was analyzed. After transfection or temozolomide (TMZ) treatment, the cell viability and apoptosis were detected using cell counting kit-8 assay and flow cytometry. The targeting relationship between LINC01410 and microRNA (miR)-370-3p was confirmed by dual-luciferase reporter assay. Expressions of LINC01410, miR-370-3p and drug resistance- and Phosphatase and Tensin Homolog (PTEN)/AKT pathway-related factors were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Results LINC01410 expression was upregulated in GBM, and silencing of LINC01410 decreased cell viability. A slowed decreased trend in cell viability yet an increased half maximal inhibitory concentration (IC50 for TMZ) value and increased expressions of drug resistance-related factors as well as LINC01410 were found in TMZ-resistant GBM cells. Silencing of LINC01410 also decreased the IC50 value yet promoted the sensitivity and apoptosis in TMZ-resistant cells, while upregulating the expression of PTEN and downregulating the phosphorylation of AKT. MiR-370-3p could competitively bind to LINC01410 and its expression was decreased in both parental and TMZ-resistant GBM cells. Downregulation of miR-370-3p reversed the effects of LINC01410 silencing on cell viability, apoptosis and the expressions of miR-370-3p and PTEN/AKT pathway-related factors. Conclusion Silencing of LINC01410 inhibits cell viability yet enhances apoptosis and sensitivity to TMZ in GBM cells by inactivating PTEN/AKT pathway via targeting miR-370-3p.