LncRNA SAMMSON Knockdown Inhibits the Malignancy of Glioblastoma Cells by Inactivation of the PI3K/Akt Pathway.

Dysregulated lncRNAs are proposed to be tightly associated with the progression of various tumors including glioblastoma (GBM). LncRNA Survival Associated Mitochondrial Melanoma-Specific Oncogenic Non-Coding RNA (SAMMSON) has been reported to be an oncogenic lncRNA in several tumors. Nevertheless, the specific role and molecular mechanism of SAMMSON in GBM progression remain unknown. Expression of SAMMSON in GBM tissues and cells was detected by qRT-PCR. CCK-8 and LDH release assays were applied to evaluate cellular viability. Invasion effect was assessed by Transwell invasion assay and western blot analysis of E-cadherin and N-cadherin expression. Apoptosis was detected using flow cytometry analysis and caspase-3 activity assay. The protein levels of phosphatidylinositol-3-kinase (PI3K), phosphorylated (p)-PI3K, protein kinase B (Akt) and p-Akt were estimated by western blot. We found that SAMMSON was highly expressed in GBM tissues and cells. SAMMSON knockdown suppressed cell viability and increased LDH release in GBM cells. Moreover, SAMMSON silencing impeded the invasive ability of GBM cells by regulating epithelial-to-mesenchymal transition (EMT). Furthermore, SAMMSON downregulation increased the apoptotic rate and caspase-3 activity in GBM cells. Additionally, it was demonstrated that the PI3K/Akt pathway was inhibited following SAMMSON silencing in GBM cells. Rescue assays revealed that activation of the PI3K/Akt pathway by 740Y-P abolished SAMMSON knockdown-induced viability reduction, invasion suppression and apoptosis in GBM cells. Taken together, lncRNA SAMMSON knockdown inhibited the malignancy of GBM cells by inactivation of the PI3K/Akt pathway.