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

Abstract

Background: 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 (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: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.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. K E Y W O R D Skeratinocytes, miR-27b, oral lichen planus, PLK2, Proliferation

Up-Regulated MicroRNA-27b Promotes Adipocyte Differentiation via Induction of Acyl-CoA Thioesterase 2 Expression

“…In addition, miR-27b highly expressed in sheep skeletal muscle directly reduced myostatin mRNA and led to cell proliferation [41]. In contrast, down-regulated miR-27b in oral lichen planus promotes human oral keratinocytes proliferation via increased Polo-like Kinase-2 expression [14]. Moreover, the down-regulation and 5: ACOT2 knockdown cancelled miR-27b-driven adipocyte di erentiation.…”

“…ese results therefore plainly indicate that the miR-27b-ACOT2 axis promotes lipid accumulation and adipocyte di erentiation, process which result in NAFLD pathogenesis. Several studies have shown that miR-27b regulates not only adipogenesis, but also cell proliferation, angiogenesis, and tumor development [14,15,40,41]. Nonetheless, the role of miR-27b has not been fully elucidated.…”

“…Among altered miRNAs in patients, we found that miR-27b is remarkedly increased in liver tissue and serum from the early phase of NAFLD to severe NASH [12,13]. It has been reported that miR-27b is involved in cell proliferation, differentiation, migration, invasion, metastasis, multi-drug resistance in various tumor cells [14][15][16][17][18]. However, the exact role of miR-27b in NAFLD pathogenesis, and in particular its relationship to adipocyte differentiation, remains unclear.…”

Vitamin D/VDR signaling induces miR-27a/b expression in oral lichen planus

“…These inconsistent observations create an unclear understanding regarding the function of miR-27. In the field of OLP, some investigations have suggested that miR-27b targets PLK2 to promote oral keratinocytes proliferation 37 . Due to the inflammatory conditions, miR-27a/b's functions may be largely involved in immune response in the context of OLP.…”

STC1 regulates glioblastoma migration and invasion via the TGF‑β/SMAD4 signaling pathway

“…By acting as ceRNAs, miRNAs are able to regulate mRNAs, long non-coding (lnc)RNAs and circular RNAs (34). Starbase is a network database used to predict mRNA or lncRNA regulation via miRNA (35,36). In the present study, it was predicted that STC-1 acted as a ceRNA of SMAD4 via miR-34a.…”