Abstract
Mounting evidences have indicated that terminal differentiation-induced lncRNA (TINCR) contributes to various cellular processes, such as proliferation, apoptosis, autophagy, migration, invasion, and metastasis. However, the function of TINCR in regulating migration of MSCs is largely unknown. In this study, the effects of TINCR on the migration of rat MSCs from the bone marrow were studied by Transwell assays and wound healing assays. Our results suggested that TINCR positively regulated migration of rMSCs. miR-761 mimics suppressed rMSC migration, whereas miR-761 inhibitor promoted migration. Target prediction analysis tools and dual-luciferase reporter gene assay identified Wnt2 as a direct target of miR-761. miR-761 could inhibit the expression of Wnt2. Further, the investigation about the function of TINCR in miR-761-induced migration of rMSCs was completed. These results demonstrated that TINCR took part in the regulation of miR-761-induced migration in rMSCs through the regulation of Wnt2 and its Wnt2 signaling pathway. Taken together, our results demonstrate that lncRNA-TINCR functions as a competitive endogenous RNA (ceRNA) to regulate the migration of rMSCs by sponging miR-761 which modulates the role of Wnt2. These findings provide evidence that lncRNA-TINCR has a chance to serve as a potential target for enhancing MSC homing through the miR-761/Wnt2 signaling pathway.
Highlights
Long noncoding RNAs are functional RNAs that lack protein-coding ability, which is more than 200 nucleotides in length
Mechanistic analysis revealed that Long noncoding RNAs (lncRNAs)-terminal differentiation-induced lncRNA (TINCR) could function as a competitive endogenous RNA to regulate the migration of rMSCs by sponging miR-761 which modulates the role of Wnt2
Being one of the important classes of noncoding RNAs, the role of numerous lncRNAs has been identified in Mesenchymal stem cells (MSCs)
Summary
Long noncoding RNAs (lncRNAs) are functional RNAs that lack protein-coding ability, which is more than 200 nucleotides in length. Some have shown that lncRNAs could function as a competing endogenous RNA (ceRNA) to sponge miRNAs, thereby preventing microRNAs from binding to their target genes [4,5,6,7]. Mechanistic analysis revealed that lncRNA-TINCR could function as a competitive endogenous RNA (ceRNA) to regulate the migration of rMSCs by sponging miR-761 which modulates the role of Wnt. Mechanistic analysis revealed that lncRNA-TINCR could function as a competitive endogenous RNA (ceRNA) to regulate the migration of rMSCs by sponging miR-761 which modulates the role of Wnt2 These findings provide evidence that lncRNA-TINCR may serve as a potential prognostic marker and therapeutic target for those MSC-relevant cancers progressing through the miR761/Wnt signaling pathway
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