Downregulated miR-27b promotes keratinocyte proliferation by targeting PLK2 in oral lichen planus.

Abstract

MicroRNA-27b (miR-27b) was recently found to be significantly downregulated in oral lichen planus (OLP). However, evidence of the function of miR-27b in OLP remains limited. Initially, miR-27b expression in OLP was verified using the quantitative real-time polymerase chain reaction (qRT-PCR). Functionally, gain-/loss-of-function studies were then conducted using miR-27b mimics/inhibitor to investigate cell growth in human oral keratinocytes (HOKs). Mechanistically, subsequent miRNA target analyses including a starBase database analysis and a luciferase reporter assay were performed to predict and validate the direct target, respectively. In addition, overexpression/knockdown assays of target(s) of miR-27b were performed to investigate its functional significance and qRT-PCR and western blotting were used to evaluate the target(s) of miR-27b mRNA and protein levels, respectively. MicroRNA-27b was significantly downregulated in OLP tissues when compared with healthy control tissues. Bioinformatics predicted that Polo Like Kinase 2 (PLK2) might be a potential target of miR-27b, while the luciferase reporter assay results showed the direct inhibition of the plk2-3'untranslated region by miR-27b. Moreover, functional analysis indicated that downregulated miR-27b caused an increase in cell growth in HOKs, and correspondingly, overexpression of PLK2 promoted HOK proliferation. There were aberrant expressions of miR-27b and PLK2 in OLP tissues. Decreased miR-27b may have induced cell proliferation by increasing the levels of PLK2 in HOKs, which provides a new perspective into the potential mechanisms underlying OLP development.