期刊
HELIYON
卷 9, 期 11, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.heliyon.2023.e21777
关键词
Glioma; Long non -coding RNA; LncBIRC3-OT; RELA; Stanniocalcin-1
This study identifies lncBIRC3-OT as an important regulator promoting the progression of glioma. Down-regulation of lncBIRC3-OT inhibits cell proliferation and invasion in glioma cells. Mechanistically, lncBIRC3-OT guides RELA protein to the STC1 promoter, initiating STC1 transcription and ultimately promoting glioma progression.
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 RNAseq 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.
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