LncRNA KCNQ1OT1 accelerates fracture healing via modulating miR‐701‐3p/FGFR3 axis. Issue 4 (14th February 2020)

• Record Type: Journal Article
• Authors: Chen, Lang; Xiong, Yuan; Yan, Chenchen; Zhou, Wu; Endo, Yori; Xue, Hang; Hu, Yiqiang; Hu, Liangcong; Leng, Xingzhu; Liu, Jing; Lin, Ze; Mi, Bobin; Liu, Guohui
• Is Part Of: FASEB journal. Volume 34:Issue 4(2020)
• Page Start: 5208
• Page End: 5222
• Publication Date: 2020-02-14
• Subjects: apoptosis -- FGFR3 -- lncRNA -- migration -- miRNA -- osteoblast proliferation; Biology -- Periodicals; Biology, Experimental -- Periodicals; 570
• DOI: 10.1096/fj.201901864RR
• Languages: English
• ISSNs: 0892-6638

Abstract

Abstract: 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.