BACKGROUND: 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 AND 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 AM-1 cells was examined using wound-healing 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 mRNA 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 AM-1 cells.

CONCLUSIONS: 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.

Keywords: Ameloblastoma, Neural Cell Adhesion Molecules, Aged, 80 and over, CD56 Antigen, Jaw Neoplasms, transcriptional activation