Non-coding RNAs are endogenous regulators of gene expression that have been implicated in the pathogenesis of various diseases, including osteoarthritis (OA). Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and miR-16-5p are up-regulated in OA tissues; however, their functions have not been clarified.
Chondrocyte ATDC5 was used as a cell model. NEAT1 overexpression and knockdown cells were established by transfection with lipofectamine. miR-16-5p was also transfected into the cells using lipofectamine. Moreover, cell proliferation was examined using cell counting kit-8 assays. Cell apoptosis was evaluated by flow cytometry. The interaction between NEAT1 and miR-16-5p was validated by a Quantitative real-time RT-PCR (qRT-PCR) and dual-luciferase reporter assays.
NEAT1 could increase cell viability and decrease apoptosis of ATDC5 cells, whereas miR-16-5p had the opposite effects. NEAT1 could specifically bind to miR-16-5p and reduce its expression.
The suppression of miR-16-5p, as mediated by NEAT1 overexpression, could promote proliferation and inhibit apoptosis of chondrocytes. It was also revealed that NEAT1 is a "double-edged sword" during the development of OA.