LncRNA-NONMMUT100923.1 regulates mouse embryonic palatal shelf adhesion by sponging miR-200a-3p to modulate medial epithelial cell desmosome junction during palatogenesis.

Cleft palate (CP) is a common neonatal craniofacial defect caused by the adhesion and fusion dysfunction of bilateral embryonic palatal shelf structures. Long non-coding RNA (lncRNA) is involved in CP formation with regulatory mechanism unknown. In this study, all-trans retinoic acid (ATRA) was used to induced cleft palate in embryonic mice as model group. The RNA-sequencing was performed to screen differentially expressed genes between the normal and model group on embryonic day 16.5, and the expression of LncRNA-NONMMUT100923.1 and miR-200a-3p, Cdsn was confirmed by RT-PCR and western blotting. Colony formation, CCK-8 and EDU assays were performed to measure cell proliferation and apoptosis on mouse embryonic palatal shelf (MEPS) epithelial cells in . Fluorescence in situ hybridization (FISH) and dual luciferase activity assays was used to investigate the regulatory effect of LncRNA-NONMMUT100923.1 on miRNA and its target genes. Up-regulation of LncRNA-NONMMUT100923.1 and while downregulation of miR-200a-3p was found in the model group. The sponging effects of LncRNA-NONMMUT100923 on miR-200a-3p and the target gene relations between and miR-200a-3p was confirmed. Low expression of miR-200a-3p was related to the increased expressed levels of and the proliferation of MEPS epithelial cells. Thus, a potential ceRNA regulatory network in which LncRNA-NONMMUT100923.1 regulates expression by competitively binding to endogenous miR-200a-3p during palatogenesis, which may inhibit MEPS adhesion by preventing the disintegration of the desmosome junction in medial edge epithelium cells. These findings indicate the regulatory role of lncRNA and provides a potential direction for target gene therapy of CP.