LINK‑A lncRNA participates in the pathogenesis of glioma by interacting with survivin
- Xia Hua
- Guangxing Li
- Zhongtao Liu
- Zhanfeng Niu
Published online on: July 1, 2019
Copyright: © Hua et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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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.