miR‑122 and miR‑199 synergistically promote autophagy in oral lichen planus by targeting the Akt/mTOR pathway.

The aim of the present study was to characterize the roles of two microRNAs (miRNAs), miR‑122 and miR‑199, in oral lichen planus (OLP). miRNA microarray analysis was performed to detect potential miRNAs involved in OLP, while in‑silicon analysis, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), western blot and immunohistochemistry (IHC) analyses were utilized to explore the molecular mechanisms underlying the roles of miR‑199 and miR‑122 in OLP. The results from the microarray and RT‑qPCR analyses demonstrated that the expression levels of miR‑122 and miR‑199 were significantly decreased in the peripheral blood mononuclear cells (PBMCs) collected from the OLP group compared with the control group. In addition, miR‑122 and miR‑199 directly targeted AKT serine/threonine kinase 1 (AKT1) and mammalian target of rapamycin (mTOR), respectively, by binding to their 3' UTRs. AKT1 and mTOR were highly expressed in PBMCs derived from OLP patients. In fact, a negative regulatory relationship was observed between miR‑122 and AKT1, and between miR‑199 and mTOR, with negative correlation coefficients of ‑0.41 and ‑0.51, respectively. Furthermore, the protein levels of AKT1, mTOR and microtubule associated protein 1 light chain 3β (LC3B) were upregulated in the OLP group compared with the control group. Finally, overexpression of miR‑122 inhibited the expression of AKT1 and LC3B, while overexpression of miR‑199 reduced the levels of mTOR and LC3B. In conclusion, the present study demonstrated that miR‑199 and miR‑122 are implicated in the pathogenesis of OLP by regulating the expression of mTOR and AKT1.