RESUMO
Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) are involved in tumor initiation and development. Recent studies illustrated that lncRNATCF7 was highly expressed in lung cancer and liver cancer, however, the expression pattern and function of lncRNATCF7 in glioma remains to be elucidated. Here, we found that lncTCF7 was highly expressed in glioma tissues and cell lines. Overexpression of lncTCF7 promoted the proliferation and migration of glioma cells. Down-regulation of lncTCF7 significantly suppressed the tumorigenesis of glioma. Mechanistically, lncTCF7 enhanced the self-renewal of glioma cells via up-regulating the expression of epithelial cell adhesion molecule (EpCAM). The detailed molecular mechanism uncovered that lncTCF7 bound to miR-200c and decreased the abundance of miR-200c, which consequently attenuated the negative regulation of miR-200c on EpCAM. Collectively, these data provide evidence to demonstrate the critical role of lncTCF7 in the tumorigeneis of glioma, which suggested that lncTCF7 might be a promising target in the treatment of glioma.
