miR-140-5p/miR-149 Affects Chondrocyte Proliferation, Apoptosis, and Autophagy by Targeting FUT1 in Osteoarthritis

被引:90
|
作者
Wang, Zi [1 ,2 ]
Hu, Jialei [1 ]
Pan, Yue [1 ]
Shan, Yujia [1 ]
Jiang, Liqun [3 ]
Qi, Xia [1 ]
Jia, Li [1 ]
机构
[1] Dalian Med Univ, Coll Lab Med, 9 Lushunnan Rd Xiduan, Dalian 116044, Liaoning, Peoples R China
[2] Dalian Municipal Cent Hosp, Dept Sports Med, Dalian 116033, Liaoning, Peoples R China
[3] Dalian Med Univ, Grad Sch, Dalian 116044, Liaoning, Peoples R China
基金
中国国家自然科学基金;
关键词
osteoarthritis; proliferation; apoptosis; autophagy; miRNAs; FUT1; MICRORNAS; CANCER; PATHOGENESIS; MECHANISM; MIGRATION; INVASION; MIR-26A; PATHWAY; MIR-149;
D O I
10.1007/s10753-018-0750-6
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Osteoarthritis (OA), the most prevalent chronic and degenerative joint disease, is characterized by articular cartilage degradation and chondrocyte injury. Increased cell apoptosis and defective cell autophagy in chondrocytes are a feature of degenerative cartilage. MicroRNAs (miRNAs) have been identified as potential regulators of OA. This study aimed to determine the potential role of miR-140-5p and miR-149 in apoptosis, autophagy, and proliferation in human primary chondrocytes and investigate the underlying mechanism. We revealed the differential expressional profiles of miR-140-5p/149 and fucosyltransferase 1 (FUT1) in the articular cartilage tissues of OA patients and normal people and validated FUT1 was a direct target of miR-140-5p/149. The overexpression of miR-140-5p/149 inhibited apoptosis and promoted proliferation and autophagy of human primary chondrocytes via downregulating FUT1. On the contrary, the downregulation of miR-140-5p/149 inhibited chondrocyte proliferation and autophagy, whereas the effect was reversed by FUT1 knockdown. Taken together, our data suggested that miR-140-5p and miR-149 could mediate the development of OA, which was regulated by FUT1. miR-140-5p/miR-149/FUT1 axis might serve as a predictive biomarker and a potential therapeutic target in OA treatment.
引用
收藏
页码:959 / 971
页数:13
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