Overexpressed TUG1 promotes self-renewal of glioma cells by functioning as a molecular sponge for miR-145, an important CSC regulator [157], in the cytoplasm and recruiting Polycomb via YY1 binding activity to repress differentiation genes in the nucleus, such as BDNF(brain derived neurotrophic factor), NGF (nerve growth factor), and NTF3 (neurotrophin 3). This evidence concerns the gene TUG1 and glioma.