Title:Linc01116 Silencing Inhibits the Proliferation and Invasion,
Promotes Apoptosis of Chordoma Cells via Regulating the
Expression of Mir-9-5p/PKG1
Volume: 24
Issue: 8
关键词:
LINC01116, miR-9-5p，脊索瘤，PGK1，糖酵解，CCK-8。
摘要:
Background: Long intergenic non-protein coding RNA 1116 (LINC01116)
plays a carcinogenic role in a variety of cancers. The study aims to investigate the roles
of LINC01116 and hsa-miR-9-5p (miR-9-5p) and fathom their interaction in chordoma.
Methods: The predicted binding sites between miR-9-5p with LINC01116 and
phosphoglycerate kinase 1 (PGK1) by starBase were confirmed through dual-luciferase
reporter assay. The behaviors of chordoma cells undergoing transfection with
siLINC01116 or miR-9-5p inhibitor were determined by Cell Counting Kit-8 (CCK-8),
colony formation, Transwell, and flow cytometry assays. The glucose consumption,
lactate production, and adenosine triphosphate (ATP) production of chordoma cells were
examined with specific kits. Quantitative real-time polymerase chain reaction (qRT-PCR)
and Western blot were performed to determine relevant gene expressions in chordoma
cells.
Results: Silencing of LINC01116 facilitated the apoptosis and expressions of Bcl-2-
associated X (Bax), cleaved caspase-3 (C caspase-3) and miR-9-5p while repressing
the cell cycle, viability, proliferation, invasion, glucose consumption, lactate production,
ATP production, and expressions of PGK1 and Bcl-2. Meanwhile, LINC01116 sponged
miR-9-5p, which could target PGK1. Moreover, the miR-9-5p inhibitor acted contrarily
and reversed the role of siLINC01116 in chordoma cells. Besides, LINC01116
downregulation facilitated apoptosis and attenuated the proliferation and invasion of
chordoma cells as well as PGK1 expression by upregulating miR-9-5p expression.
Conclusion: LINC01116/miR-9-5p plays a regulatory role in the progression of
chordoma cells and is a potential biomarker for chordoma.
