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Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults that originates from glial cells. The prognosis of patients with high‑grade glioma is poor. It is therefore crucial to develop effective therapeutic strategies. Long non‑coding RNAs (lncRNAs) have been reported as potential inducers or suppressors of tumor progression. Previous studies have indicated that the lncRNA Feline Leukemia Virus Subgroup C Cellular Receptor 1 Antisense RNA 1 (FLVCR1‑AS1) is involved in the development and progression of gastric and lung cancer, as well as hepatocellular carcinoma and cholangiocarcinoma; however, the biological effect of FLVCR1‑AS1 in glioma is not completely understood. The aim of the present study was to investigate how FLVCR1‑AS1 modulates cell proliferation and invasion in glioma. FLVCR1‑AS1 expression was significantly upregulated in GBM tissues compared with adjacent normal brain samples, and was higher in GBM cell lines compared with normal human astrocyte cells. Furthermore, the microRNA (miR)‑30b‑3p was revealed to be a putative target of FLVCR1‑AS1, and the suppressive effects of miR‑30b‑3p on cellular proliferation and invasion were reversed following FLVCR1‑AS1‑knockdown. The results from Cell Counting Kit‑8 and Transwell assays confirmed that FLVCR1‑AS1‑knockdown inhibited GBM cell proliferation and invasion ability. In addition, FLVCR1‑AS1 was found to directly interact with miR‑30b‑3p, and a rescue experiment further established that FLVCR1‑AS1 contributed to glioma progression by inhibiting miR‑30b‑3p. The results from the present study demonstrated that FLVCR1‑AS1 may serve an oncogenic role in GBM and promote disease progression by interacting with miR‑30b‑3p. These findings suggested that FLVCR1‑AS1 may be considered as a novel therapeutic target and diagnostic biomarker for GBM.

It was reported that γ-irradiation had a controversial therapeutic effect on glioma cells. We aimed to investigate the cytotoxic effect on the glioma cells induced by γ-irradiation and explore the treatment to rescue the phenotype alteration of remaining cells. We used transwell assay to detect the glioma cell invasion and migration capacity. Cell proliferation and apoptosis were tested by the CCK-8 assay and flow cytometry respectively. Western Blot was used to detect the activity of Hedgehog signaling pathway and Epithelial-to-Mesenchymal Transition (EMT) status. γ-irradiation showed cytotoxic effect on LN229 cells in vitro, whereas this contribution was limited in U251 cells. However, it could significantly stimulated EMT process in both LN229 and U251. Curcumin (CCM) could rescue EMT process induced by γ-irradiation via the suppression of Gli1 and the upregulation of Sufu. The location and expression of EMT markers were also verified by Immunofluorescence. Immunohistochemistry assay was used on intracranial glioma tissues of nude mice. The capacities of cell migration and invasion were suppressed with combined therapy. This research showed Curcumin could rescue the EMT process induced by γ-irradiation via inhibiting the Hedgehog signaling pathway and potentiate the cell cytotoxic effect in vivo and in vitro.