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

doi:10.1016/j.heliyon.2023.e21777

LncBIRC3-OT promotes the malignant progression of glioma by interacting with RELA to upregulate stanniocalcin-1 expression

Heliyon. 2023 Nov 4;9(11):e21777. doi: 10.1016/j.heliyon.2023.e21777. eCollection 2023 Nov.

Authors

Renjie Wang^{1

2}, Qi Li¹, Xiaolei Chu¹, Nan Li², Haiqian Liang², Feng He¹

Affiliations

¹ Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, 300072, China.
² Institute of Traumatic Brain Injury and Neurology, Characteristic Medical Center of Chinese People's Armed Police Force, Tianjin, 300162, China.

Abstract

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.

Keywords: Glioma; LncBIRC3-OT; Long non-coding RNA; RELA; Stanniocalcin-1.