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Downregulated miR‐27b promotes keratinocyte proliferation by targeting PLK 2 in oral lichen planus
Author(s) -
Chen Junjun,
Du Guanhuan,
Chang Yuzhou,
Wang Yufeng,
Shi Linjun,
Mi Jun,
Tang Guoyao
Publication year - 2019
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12826
Subject(s) - gene knockdown , microrna , cell growth , messenger rna , downregulation and upregulation , blot , cell , three prime untranslated region , microbiology and biotechnology , untranslated region , cancer research , luciferase , chemistry , biology , cell culture , transfection , gene , biochemistry , genetics
Background Micro RNA ‐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 ). Functionally, gain‐/loss‐of‐function studies were then conducted using miR‐27b mimics/inhibitor to investigate cell growth in human oral keratinocytes ( HOK s). Mechanistically, subsequent mi RNA 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 Micro RNA ‐27b was significantly downregulated in OLP tissues when compared with healthy control tissues. Bioinformatics predicted that Polo Like Kinase 2 ( PLK 2) 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 HOK s, and correspondingly, overexpression of PLK 2 promoted HOK proliferation. Conclusions There were aberrant expressions of miR‐27b and PLK 2 in OLP tissues. Decreased miR‐27b may have induced cell proliferation by increasing the levels of PLK 2 in HOK s, which provides a new perspective into the potential mechanisms underlying OLP development.