The lncRNA RP11-142A22.4 promotes adipogenesis by sponging miR-587 to modulate Wnt5β expression

• Published in: Cell death & disease 2020-06, Vol.11 (6), p.475-475, Article 475
• Main Authors: Zhang, Tongtong, Liu, Hongtao, Mao, Rui, Yang, Huawu, Zhang, Yuanchuan, Zhang, Yu, Guo, Pengsen, Zhan, Dafang, Xiang, Bin, Liu, Yanjun
• Format: Article
• Language: English
• Subjects: 38; 38/109; 38/61; 45; 45/77; 631/337; 631/80; Adipocytes - metabolism; Adipocytes - pathology; Adipogenesis; Adipogenesis - genetics; Adipose tissue; Adult; Antibodies; Base Sequence; Binding sites; Biochemistry; Biomedical and Life Sciences; CCAAT/enhancer-binding protein; Cell Biology; Cell Culture; Cell Differentiation - genetics; Female; Gene expression; Gene Expression Profiling; Gene Expression Regulation; Gene Knockdown Techniques; Humans; Immunology; Intra-Abdominal Fat - metabolism; Life Sciences; Male; MicroRNAs - genetics; MicroRNAs - metabolism; Obesity - genetics; Peroxisome proliferator-activated receptors; Preadipocytes; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Signal Transduction; Up-Regulation - genetics; Wnt Proteins - genetics; Wnt Proteins - metabolism
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-020-2550-9

Emerging evidence suggests that long noncoding RNAs (lncRNAs) play essential roles in the regulation of gene expression. However, the functional contributions of lncRNAs to adipogenesis remain largely unexplored. In this study, we investigated global changes in the expression patterns of lncRNAs in visceral adipose tissue and identified RP11-142A22.4 as a significantly upregulated lncRNA. In isolated preadipocytes, knockdown of RP11-142A22.4 inhibited differentiation and reduced C/EBP-α and PPAR-γ expression. Investigations of the underlying mechanisms revealed that RP11-142A22.4 contains a functional miR-587 binding site. Mutation of the binding sites for RP11-142A22.4 in miR-587 abolished the interaction, as indicated by a luciferase reporter assay. Furthermore, RP11-142A22.4 affected the expression of miR-587 and its target gene Wnt5β. Overexpression of miR-587 blocked the inhibitory effect of RP11-142A22.4 on preadipocyte differentiation. Moreover, the downregulation of miR-587 restored preadipocyte differentiation upon inhibition by RP11-142A22.4 silencing. Our results suggest that RP11-142A22.4 can control adipocyte differentiation via the miR-587/Wnt5β signaling pathway and serve as a potential target for obesity treatments.