Long non‑coding RNA MEG3 contributes to cisplatin‑induced apoptosis via inhibition of autophagy in human glioma cells.

Long non-coding RNAs (lncRNAs) function as oncogenes or tumor suppressors, and are involved in mediating tumorigenesis and resistance to chemotherapy by altering the expression of genes at various levels. Accumulating evidence suggests that the maternally expressed gene 3 (MEG3) lncRNA serves an important role in a number of cancers. However, its functional role in mediating cisplatin‑induced apoptosis of glioma cells is unknown. To investigate the role of MEG3, the mRNA levels of MEG3 under cisplatin treatment were investigated by reverse transcription‑quantitative polymerase chain reaction, and the cell viability and apoptosis were examined by MTT assay, and flow cytometry analysis and western blotting, respectively. The results demonstrated that MEG3 expression levels were increased in U87 cells following cisplatin treatment. Elevated MEG3 by lentiviral transfection enhanced the chemosensitivity of U87 cells to cisplatin, whereas knockdown of MEG3 expression by small interfering RNA transfection increased the resistance of U87 cells to cisplatin. Subsequent mechanistic studies revealed that MEG3 eliminated autophagy induced by cisplatin. Decreased MEG3‑induced autophagy improved the chemosensitivity of U87 cells to cisplatin. The results present a novel therapeutic strategy for the treatment of patients with glioblastoma multiforme.