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

Abstract

Background

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.

Methods

Initially, miR‐27b expression in OLP was verified using the quantitative real‐time polymerase chain reaction (qRT‐PCR). Functional, 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.

Results

miR‐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 of cell growth in HOKs, and correspondingly, overexpression of PLK2 promoted HOK proliferation.

Conclusions

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.

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