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

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.