ArticleInternational journal of molecular medicine2019
miR‑122 and miR‑199 synergistically promote autophagy in oral lichen planus by targeting the Akt/mTOR pathway.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- PstS1-loaded exosomes promote Mycobacterium tuberculosis infection via miR-122-mediated PI3K/AKT/mTOR activation and autophagy suppression.In vitro cellular & developmental biology. Animal · 2026Article
- The Expression and Potential Role of MicroRNAs in Oral Lichen Planus.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026Article
- Oxidative stress and metabolic dysfunction in oral lichen planus pathogenesis.Animal cells and systems · 2026Review
- Epimedium Brevicornu and Curculigo orchioides inhibit osteoclast autophagy by degrading the level of miRNA-199 to regulate the mTOR signaling pathway.Journal of orthopaedic surgery and research · 2025Article
- Autophagy as a potential therapeutic target in regulating improper cellular proliferation.Frontiers in pharmacology · 2025Review
- The role of MicroRNAs in the diagnosis and treatment of oral premalignant disorders.Odontology · 2024Review
- Article
- Unveiling the Potential of Serum MiR-483-5p: A Promising Diagnostic and Prognostic Biomarker in OLP and OSCC Patients byCurrent pharmaceutical design · 2024Article
- Review
- The role of altered microRNA expression in premalignant and malignant head and neck lesions with epithelial origin.Health science reports · 2022Article
- Hallmarks of Cancer Expression in Oral Lichen Planus: A Scoping Review of Systematic Reviews and Meta-Analyses.International journal of molecular sciences · 2022Article
- The Immunogenetics of Lichen Planus.Advances in experimental medicine and biology · 2022Article
- The Functional Mechanism of MicroRNA in Oral Lichen Planus.Journal of inflammation research · 2022Review
- MicroRNA-122 promotes apoptosis of keratinocytes in oral lichen planus through suppressing VDR expression.Journal of cellular and molecular medicine · 2021Article
- Noncoding RNAs in oral premalignant disorders and oral squamous cell carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020Review
- Nicotinamide: Oversight of Metabolic Dysfunction Through SIRT1, mTOR, and Clock Genes.Current neurovascular research · 2020Review
- Dysregulation of metabolic flexibility: The impact of mTOR on autophagy in neurodegenerative disease.International review of neurobiology · 2020Review
- Prognostic and Therapeutic Potentials of OncomiRs Modulating mTOR Pathways in Virus-Associated Hepatocellular Carcinoma.Frontiers in oncology · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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