LncRNA KCNQ1OT1 accelerates fracture healing via modulating miR-701-3p/FGFR3 axis

被引:38
作者
Chen, Lang [1 ]
Xiong, Yuan [1 ]
Yan, Chenchen [1 ]
Zhou, Wu [1 ]
Endo, Yori [2 ]
Xue, Hang [1 ]
Hu, Yiqiang [1 ]
Hu, Liangcong [1 ]
Leng, Xingzhu [3 ]
Liu, Jing [1 ]
Lin, Ze [1 ]
Mi, Bobin [1 ]
Liu, Guohui [1 ]
机构
[1] Huazhong Univ Sci & Technol, Union Hosp, Dept Orthoped, Tongji Med Coll, Wuhan, Peoples R China
[2] Harvard Med Sch, Brigham & Womens Hosp, Div Plast Surg, Boston, MA 02115 USA
[3] Univ Utrecht, Dept Biomed Sci, UMC Utrecht, Utrecht, Netherlands
基金
中国国家自然科学基金;
关键词
apoptosis; FGFR3; lncRNA; migration; miRNA; osteoblast proliferation; ENDOCHONDRAL OSSIFICATION; FGFR3; RNA; MOUSE;
D O I
10.1096/fj.201901864RR
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
Emerging evidence highlights the role of the long noncoding RNA (lncRNA) KCNQ1OT1 in fracture healing. Osteoblast proliferation, migration, and survival are pivotal during this process. In this study, we aimed to improve our understanding of the regulatory role of lncRNA KCNQ1OT1 during osteoblast proliferation, migration, and survival. We searched the gene expression omnibus databases and LncBase Experimental V.2 to identify key microRNAs (miRNAs) targets of KCNQ1OT1. MiR-701-3p was selected as a differentially expressed miRNA and RNA immunoprecipitation assays were performed to verify its interaction with KCNQ1OT1. Fibroblast growth factor receptor 3 (FGFR3) was also identified as a target of miR-701-3p. We further identified KCNQ1OT1 as a competing endogenous RNA of miR-701-3p that could influence osteoblast proliferation, migration, and apoptosis in vitro and in vivo. Taken together, our results indicate that the KCNQ1OT1/miR-701-3p/FGFR3 axis is an important regulator of osteoblast proliferation, migration, and apoptosis, and provide a new therapeutic avenue for fracture healing.
引用
收藏
页码:5208 / 5222
页数:15
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