Premium
LncRNA NEAT1 promotes proliferation of chondrocytes via down‐regulation of miR‐16‐5p in osteoarthritis
Author(s) -
Li Dan,
Sun Yongjin,
Wan Yunpeng,
Wu Xing,
Yang Wanrong
Publication year - 2020
Publication title -
the journal of gene medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 91
eISSN - 1521-2254
pISSN - 1099-498X
DOI - 10.1002/jgm.3203
Subject(s) - lipofectamine , gene knockdown , transfection , apoptosis , cell growth , viability assay , competing endogenous rna , flow cytometry , chondrocyte , microbiology and biotechnology , cell , reporter gene , luciferase , biology , chemistry , cell culture , long non coding rna , gene expression , downregulation and upregulation , cartilage , gene , biochemistry , genetics , vector (molecular biology) , anatomy , recombinant dna
Background 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. Methods 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. Results 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. Conclusions 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.