RETRACTED: Long non-coding RNA reprogramming (lncRNA-ROR) regulates cell apoptosis and autophagy in chondrocytes (Retracted article. See vol. 122, 2021)

被引:43
|
作者
Yang, Zhongmeng [1 ]
Tang, Yuxing [1 ]
Lu, Huading [1 ]
Shi, Bo [1 ]
Ye, Yongheng [1 ]
Xu, Guoyong [1 ]
Zhao, Qing [1 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 5, Dept Orthoped, 52 Meihua East Rd, Zhuhai 519000, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
apoptosis; cell viability; long non-coding RNA ROR; p53; osteoarthritis; CARTILAGE; CANCER; PROLIFERATION; PROMOTES; EXPRESSION; OSTEOARTHRITIS; CASPASE-3; INVASION; HOTAIR; GROWTH;
D O I
10.1002/jcb.27057
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Long Non-Coding RNA Reprogramming (lncRNA-ROR) plays an important role in regulating various biologic processes, whereas the effect of lncRNA-ROR in osteoarthritis (OA) is little studied. This study aimed to explore lncRNA-ROR expression in articular cartilage and identify the functional mechanism of lncRNA-ROR in OA. OA cartilage tissues were obtained from 15 OA patients, and 6 normal cartilage tissues were set as controls. Chondrocytes were isolated from the collected cartilage tissues. lncRNA-ROR was knockdown in normal cells and overexpressed in OA cells. Cell viability was determined with Cell Counting Kit-8 assay, and apoptosis was measured using flow cytometric analysis. Moreover, proteins and mRNAs involved in this study were also measured using Western blotting and quantitative real-time PCR (qPCR). Level of lncRNA-ROR was decreased in OA compared with normal chondrocytes, and overexpression of lncRNA-ROR dramatically promoted cell viability of OA chondrocytes. In addition, knockdown lncRNA-ROR inhibited apoptosis and promoted autophagy of normal chondrocytes. Moreover, lncRNA-ROR inhibited the expression of p53 in both mRNA and protein levels. Furthermore, we revealed that lncRNA-ROR regulated apoptosis and autophagy of chondrocytes via HIF1 and p53. The results indicated that lncRNA-ROR played a critical role in the pathogenesis of OA, suggesting that lncRNA-ROR could serve as a new potential therapeutic target for OA.
引用
收藏
页码:8432 / 8440
页数:9
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