Up-regulated Neural Cell Adhesion Molecule(NCAM1) By Hsa-miR-141-3p Suppresses Ameloblastoma Cell Migration

Objective: Neural cell adhesion molecule 1(NCAM1;CD56)and E-cadherin are both involved in cell-cell adhesion and cell development processes,and their dysregulation is associated with various tumors.We hypothesized that dysregulated NCAM1 could suppress the invasive behavior of ameloblastoma(AB),and its expression was regulated by miR-141-3p.Material/Methods: Real-time qPCR was performed to examine differences in miR-141-3p expression between AB tissues and normal oral tissues(NOMs).The potential target NCAM1 of miR-141-3p was predicted by bioinformatics analysis,which was validated through dual-luciferase assay.The mRNA and protein levels of NCAM1 were detected by real-time qPCR and Western blot,respectively.Furthermore,the expression and distribution of NCAM1 in AB were investigated through immunohistochemical staining,and immunohistochemical staining of E-cadherin was also performed.After overexpression of NCAM1,the migration of HAM-1 cells was examined using woundhealing assay.Results: Real-time qPCR results confirmed that miR-141-3p was significantly downregulated in AB tissues.According to bioinformatics analysis,NCAM1 was a target of miR-141-3p,which was confirmed by dual luciferase assay.We found that NCAM1 was significantly upregulated in AB tissues at the m RNA and protein levels.Furthermore,NCAM1 and E-cadherin were mainly expressed on the cell membrane of AB.Downregulation of E-cadherin was found in AB tissues.As shown in wound-healing assay results,NCAM1 overexpression significantly inhibited the invasiveness of HAM-1 cells.Conclusion: In this study,highly expressed NCAM1 was found in AB,and it suppressed the migration of AB cells and was regulated by miR-141-3p,suggesting its potential value as a therapeutic target for AB.