ArticleCommunications biology2023
METTL14-upregulated miR-6858 triggers cell apoptosis in keratinocytes of oral lichen planus through decreasing GSDMC.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Deletion of NFIA Leads to Activation of S100A7 and Inflammatory Response-Induced Apoptosis of Keratinocytes in Oral Lichen Planus Progression.The Kaohsiung journal of medical sciences · 2025Article
- RNA modifications at the heart of oral inflammation.Molecular therapy. Nucleic acids · 2025Article
- Etiopathogenesis of Oral Lichen Planus: A Review.Head and neck pathology · 2025Review
- FTO deficiency facilitates epithelia dysfunction in oral lichen planus.Molecular therapy. Nucleic acids · 2025Article
- Review
- Unraveling the landscape of m6A RNA methylation in wound healing and scars.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral lichen planus (OLP), a chronic inflammatory disorder, is characterized by the massive cell apoptosis in the keratinocytes of oral mucosa. However, the mechanism responsible for triggering oral keratinocyte apoptosis is not fully explained. Here, we identify that Gasdermin C (GSDMC) downregulation contributes to apoptosis in human oral keratinocytes. Mechanistically, we describe that activated nuclear factor kappa B (NF-κB) pathway induces overexpression of methyltransferase-like 14 (METTL14), which increases N
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Registered trials
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