[No authors listed]
Glioblastoma (GBM) is the most common and malignant primary brain tumor in adults that originates from glial cells. The prognosis of patients with highâgrade glioma is poor. It is therefore crucial to develop effective therapeutic strategies. Long nonâcoding 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 1 (FLVCR1âAS1) is involved in the development and progression of gastric and lung cancer, as well as hepatocellular carcinoma and cholangiocarcinoma; however, the biological effect of FLVCR1âAS1 in glioma is not completely understood. The aim of the present study was to investigate how FLVCR1âAS1 modulates cell proliferation and invasion in glioma. FLVCR1âAS1 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)â30bâ3p was revealed to be a putative target of FLVCR1âAS1, and the suppressive effects of miRâ30bâ3p on cellular proliferation and invasion were reversed following FLVCR1âAS1âknockdown. The results from Cell Counting Kitâ8 and Transwell assays confirmed that FLVCR1âAS1âknockdown inhibited GBM cell proliferation and invasion ability. In addition, FLVCR1âAS1 was found to directly interact with miRâ30bâ3p, and a rescue experiment further established that FLVCR1âAS1 contributed to glioma progression by inhibiting miRâ30bâ3p. The results from the present study demonstrated that FLVCR1âAS1 may serve an oncogenic role in GBM and promote disease progression by interacting with miRâ30bâ3p. These findings suggested that FLVCR1âAS1 may be considered as a novel therapeutic target and diagnostic biomarker for GBM.
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