ArticleJournal of cellular and molecular medicine2021
MicroRNA-122 promotes apoptosis of keratinocytes in oral lichen planus through suppressing VDR expression.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Epigenetic Therapies for Inflammatory and Immune-Mediated Skin Diseases.Biomedicines · 2026Review
- Overexpression of miR-516a-5p Promotes Erosive Oral Lichen Planus: In Vitro Study Based on Bioinformatics Analyses.Clinical and experimental dental research · 2025Article
- Salivary MicroRNAs as Innovative Biomarkers for Diagnosis and Prediction of the Oral Potentially Malignant Disorders Transition Towards Oral Cancer: A Systematic Review.Journal of clinical medicine · 2025Review
- Oral Lichen Planus: A Narrative Review Navigating Etiologies, Clinical Manifestations, Diagnostics, and Therapeutic Approaches.Journal of clinical medicine · 2024Review
- Role of Vitamin D in Oral Lichen Planus: A Case Control Study.Nutrients · 2024Article
- Association between Vitamin D Receptor Polymorphism and Susceptibility to Oral Lichen Planus and Oral Squamous Cell Carcinoma.Iranian journal of otorhinolaryngology · 2024Article
- Review
- Comprehensive Insight into Lichen Planus Immunopathogenesis.International journal of molecular sciences · 2023Review
- 1,25(OH)Journal of cellular and molecular medicine · 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
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
MicroRNA-122 (miR-122) is known to be up-regulated by inflammation to exert a variety of biological functions in hepatocellular carcinoma (HCC)-derived human cell lines. Vitamin D receptor (VDR) is reported to regulate excessive oral keratinocytes apoptosis which compromises oral epithelial barrier in oral lichen planus (OLP). Although many studies have suggested that miR-122 is capable of regulating cell apoptosis, its effects on the development of OLP and VDR expression are still unclear. Herein, we demonstrate that miR-122 expression is increased in the epithelial layer of OLP. Mechanically, transcription factor nuclear factor-κB (NF-κB) selectively binds with κB element in the promoter of miR-122 to accelerate gene transcription. The up-regulation of miR-122 induces cell apoptosis in human oral keratinocytes (HOKs) by targeting VDR mRNA. In VDR knockout oral keratinocytes, miR-122 fails to improve caspase 3 activity and cleaved caspase 3 and poly(ADP-ribose) polymerase (PARP) levels. Moreover, VDR overexpression is able to reverse lipopolysaccharide (LPS)- or activated CD4+ T cell-induced miR-122 up-regulation and ameliorate miR-122-stimulated caspase 3 activity. Collectively, our results suggest that miR-122 promotes oral keratinocytes apoptosis in OLP through decreasing VDR expression.
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Registered trials
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