mRNA and lncRNA expression profiles as potential targets for diagnosis and treatment of oral lichen planus.

OBJECTIVE

This study aimed to identify differentially expressed (DE) mRNAs and long noncoding RNAs (lncRNAs) between oral lichen planus (OLP) and skin lichen planus (SLP) to elucidate the molecular mechanisms driving the higher malignant transformation risk associated with OLP.

DESIGN

Tissue samples were collected from SLP and OLP patients who were diagnosed at between 2008 and 2012. RNA sequencing was conducted to analyze the differentially expressed (DE) mRNAs and lncRNAs in OLP compared to SLP. We performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA), and Protein-Protein Interaction (PPI) Network analyses using the identified DE mRNAs in OLP.

RESULTS

Analysis revealed 1106 OLP-specific DE mRNAs (555 upregulated) and 348 DE lncRNAs (201 upregulated). KEGG and GSEA highlighted significant enrichment in IL-17 and TNF-α/NF-κB signaling pathways. PPI network analysis identified key hub genes (CXCL1, CXCL2, CXCL8, JUN, IL1B, IL6) linked to IL-17 signaling. Notable dysregulation included upregulated oncogenic lncRNAs (H19, MIR31HG, SNHG15) and downregulated tumor suppressors (CA3-AS1, HAND2-AS1). Furthermore, 1228 co-expressed lncRNA-mRNA pairs were identified through trans-target prediction.

CONCLUSION

The identified DE mRNAs enriched in IL-17 and TNF-α/NF-κB signaling pathways, along with the dysregulation of oncogenic and tumor suppressor lncRNAs, provide molecular evidence for the higher risk of malignant transformation associated with OLP compared to SLP. These DE mRNAs and lncRNAs, along with their target genes, represent potential novel biomarkers or therapeutic targets for the diagnosis and management of OLP.