LINK‑A lncRNA participates in the pathogenesis of glioma by interacting with survivin

Abstract

Long intergenic non-coding RNA for kinase activation (LINK-A) long non-coding RNA (lncRNA) has been characterized in triple negative breast cancer, but its potential involvement in glioma has not been investigated. In the present study, serum levels of LINK-A lncRNA and survivin in patients with glioma and healthy controls were determined by RT-qPCR and ELISA, respectively. The diagnostic value of serum LINK-A lncRNA for glioma was evaluated by receiver operating characteristic (ROC) curve analysis. Potential correlations between serum levels of LINK-A lncRNA and survivin were analyzed by Pearson correlation coefficient. LINK-A lncRNA siRNA, LINK-A lncRNA-carrying expression vector and survivin-carrying expression vector were transfected into glioma cells, and the effects on LINK-A lncRNA expression, survivin expression and cell apoptosis were explored by RT-qPCR, western blot analysis and annexin V/propidium iodide staining. It was observed that the serum levels of LINK-A lncRNA and survivin were significantly higher in patients with glioma compared with healthy controls. Increased levels of LINK-A lncRNA distinguished glioma patients from healthy controls, based on ROC curve analysis. Serum levels of LINK-A lncRNA and survivin were positively correlated in glioma patients, but not in healthy controls. Overexpression of LINK-A lncRNA led to increased survivin protein expression, while survivin overexpression had no effect on LINK-A lncRNA expression. LINK-A lncRNA and survivin overexpression each reduced glioma cell apoptosis, but LINK-A lncRNA siRNA-mediated knockdown increased apoptosis. Survivin overexpression attenuated the inducing effects of LINK-A lncRNA knockdown on apoptosis. In conclusion, LINK-A lncRNA inhibited glioma cell apoptosis potentially by the upregulation of survivin. The present study revealed that LINK-A may serve as possible diagnostic marker for glioma.