Department of Neurosurgery, Cangzhou People's Hospital, He Bei, 061000, China.
Department of Neurosurgery, Cangzhou People's Hospital, He Bei, 061000, China.
Biomed Pharmacother. 2018 Jan;97:203-208. doi: 10.1016/j.biopha.2017.10.039. Epub 2017 Nov 6.
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.
越来越多的证据表明，长非编码 RNA（lncRNA）参与了肿瘤的发生和发展。最近的研究表明，lncRNATCF7 在肺癌和肝癌中高度表达，然而，lncRNATCF7 在神经胶质瘤中的表达模式和功能仍有待阐明。在这里，我们发现 lncTCF7 在神经胶质瘤组织和细胞系中高度表达。lncTCF7 的过表达促进了神经胶质瘤细胞的增殖和迁移。lncTCF7 的下调显著抑制了神经胶质瘤的致瘤性。机制上，lncTCF7 通过上调上皮细胞黏附分子（EpCAM）的表达增强了神经胶质瘤细胞的自我更新能力。详细的分子机制表明，lncTCF7 结合 miR-200c 并降低 miR-200c 的丰度，从而减弱 miR-200c 对 EpCAM 的负调控。总之，这些数据提供了证据，证明 lncTCF7 在神经胶质瘤的肿瘤发生中起着关键作用，这表明 lncTCF7 可能是治疗神经胶质瘤的一个有前途的靶点。
