Our study revealed that LINC00665 is downregulated in glioma tissues and cells, and overexpression of LINC00665 inhibited the malignant biological behaviors of glioma cells. In previous studies, LINC00665 functioned as an oncogene in non-small-cell lung cancer and lung adenoma and was associated with poor prognosis in hepatocellular carcinoma.33, 34, 35 However, a recent study indicated that LINC00665 knockdown promoted migration and invasion in triple-negative breast cancer MDA-MB-231 cells, which is consistent with our experimental results.36 Likewise, lncRNA GAS5 is downregulated in glioma, breast cancer, and hepatocellular carcinoma, but it promotes proliferation, migration, and invasion by regulation of miR-301a in esophageal cancer.37, 38, 39, 40 These results suggest that the same lncRNA may show differential gene expression and contribute to inverse functions in different cancers. At present, dysregulation of lncRNAs has emerged as an important component in cellular processes and tumorigenesis. Our previous studies provided some insight into the regulatory mechanisms of various lncRNAs on the biological behaviors of glioma cells. PVT1, which is overexpressed in glioma, was found to promote glioma cell survival by sponging miR-190a-5p and miR-488-3p; HOXA-AS2 increased
