Long Noncoding RNA TUNAR Represses Growth, Migration, and Invasion of Human Glioma Cells Through Regulating miR-200a and Rac1 (Withdrawn Publication)

Glioma is the most common primary adult brain tumor. Mounting research has illustrated the function of long noncoding RNAs (lncRNAs) in glioma progress, but almost no studies have reported the role of TCL1 upstream neural differentiation-associated RNA (TUNAR) in glioma cells. This study aimed to investigate the function of TUNAR in glioma. The GL15 cell line was used in this study. The interactions between TUNAR and miR-200a, or miR-200a and Rac1 were determined by cotransfection experiments. TUNAR overexpression significantly inhibited glioma malignancy by decreasing cell viability, migration, and invasion and promoting cell apoptosis. TUNAR was confirmed to positively regulate miR-200a, and knockdown of miR-200a reversed the TUNAR-induced inhibitory effects on glioma cells. Further, Rac1 was negatively regulated by miR-200a. Rac1 overexpression abolished miR-200a overexpression-induced inhibition of viability, migration, and invasion, as well as the increase in apoptosis. Rac1 knockdown inhibited glioma by inactivating the Wnt/beta-catenin and NF-kappa B signaling pathways. Our findings suggested that TUNAR played an anticancer role in glioma cells by upregulating miR-200a and inhibiting Rac1, and so might represent a potential therapeutic target for the treatment of human glioma.