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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.

Mutations in ATRX constitute the most prevalent genetic abnormalities in gliomas. The presence of ATRX mutations in glioma serves as a marker of better prognosis with longer patient survival although the underlying mechanisms are poorly understood. In the present study, we found that ATRX biological function was significantly involved in DNA replication and repair. CRISPR/Cas9-mediated genetic inactivation of ATRX induced inhibition of cell proliferation, invasion and vasculogenic mimicry. In addition, temozolomide (TMZ) treatment induced greater DNA damage and apoptotic changes in ATRX knockout glioma cells. Moreover, we confirmed that ATRX knockout resulted in a failure to trigger ATM phosphorylation and finally restrained the activation of downstream proteins of the ATM pathway. The ATM-associated DNA repair pathway was extensively compromised in ATRX knockout cells owing to decreased histone H3K9me3 availability. Public databases also showed that patients with low ATRX expression exhibited preferable overall survival and profited more from TMZ treatment. These data suggest that ATRX is involved in DNA damage repair by regulating the ATM pathway and might serve as a prognostic maker in predicting TMZ chemosensitivity. [ABSTRACT FROM AUTHOR]