LncBIRC3-OT promotes the malignant progression of glioma by interacting with RELA to upregulate stanniocalcin-1 expression
Renjie Wang,
Qi Li,
Xiaolei Chu,
Nan Li,
Haiqian Liang,
Feng He
Affiliations
Renjie Wang
Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, 300072, China; Institute of Traumatic Brain Injury and Neurology, Characteristic Medical Center of Chinese People's Armed Police Force, Tianjin, 300162, China
Qi Li
Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, 300072, China
Xiaolei Chu
Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, 300072, China
Nan Li
Institute of Traumatic Brain Injury and Neurology, Characteristic Medical Center of Chinese People's Armed Police Force, Tianjin, 300162, China
Haiqian Liang
Institute of Traumatic Brain Injury and Neurology, Characteristic Medical Center of Chinese People's Armed Police Force, Tianjin, 300162, China; Corresponding author. Characteristic Medical Center of Chinese People's Armed Police Force, Tianjin, 300162, China.
Feng He
Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, 300072, China; Corresponding author. Tianjin University, Tianjin, 300162, China.
Glioma is the most common malignant intracranial tumor, accounting for 80 % of all malignant brain tumors. Growing evidence suggests that lncRNAs are involved in the growth, angiogenesis, metastasis, and therapeutic resistance in a variety of tumors, including glioma. In this study, lncBIRC3-OT (NONHSAT159592.1), which is highly expressed in glioma, was screened by RNA-seq method and verified by quantitative reverse transcription polymerase chain reaction. Subsequently, we knocked down the endogenous expression of lncBIRC3-OT in U87 and U251 cells and found that down-regulated lncBIRC3-OT inhibited cell proliferation, colony formation, migration, and invasion. Mechanically, lncBIRC3-OT could guide RELA protein to the stanniocalcin-1 (STC1) promoter, initiate STC1 transcription, and ultimately promote the progression of glioma. Together, these findings suggest that lncBIRC3-OT is an important regulator promoting glioma progression, and may be a promising therapeutic target for glioma.
