SCIN Overexpression Attenuates LPS-Induced Apoptosis and Differentially Modulates EGFR Abundance and Phosphorylation in Human Oral Keratinocytes

Background: Oral lichen planus (OLP) is a chronic inflammatory and immune-mediated oral mucosal disease characterized by epithelial damage, basal cell degeneration, and recurrent lesions. However, the molecular mechanisms responsible for keratinocyte injury and apoptosis during OLP progression remain incompletely understood. This study aimed to investigate the protective role of scinderin (SCIN) and the potential involvement of epidermal growth factor receptor (EGFR) signaling during lipopolysaccharide (LPS)-induced inflammatory stress in human oral keratinocytes (HOKs).Methods: HOKs underwent transfection and were treated with LPS. Relative 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) metabolic activity and apoptosis were evaluated using an MTT assay and flow cytometry. Apoptosis-related proteins were assessed using Western blotting. Caspase 3 and 9 activities were assessed using a fluorometric assay. SCIN expression was analyzed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting, whereas total EGFR, inhibitor of nuclear factor kappa B alpha (IκBα), and their phosphorylated forms were evaluated by Western blotting.Results: LPS stimulation decreased SCIN and total EGFR protein levels and relative MTT metabolic activity while increasing p-EGFR protein levels and p-EGFR/EGFR ratios (p < 0.001). LPS also promoted apoptosis, as evidenced by an increased apoptotic rate, elevated BCL-2-associated X protein (BAX) expression, cleaved caspase 3/caspase 3 ratio, and caspase 3 and caspase 9 activities, as well as decreased B-cell lymphoma 2 (BCL-2) expression (p < 0.05). SCIN overexpression significantly counteracted these LPS-induced molecular and cellular changes (p < 0.05). Compared with the Control group, LPS treatment also increased the phosphorylated (p)-IκBα/IκBα ratio (p < 0.001). EGFR knockdown further aggravated LPS-induced injury, whereas SCIN overexpression partially alleviated the associated apoptotic changes under EGFR knockdown conditions (p < 0.05).Conclusion: SCIN overexpression alleviated LPS-induced apoptosis in HOKs and was associated with changes in EGFR expression and phosphorylation. These findings highlight SCIN as a potential regulator of keratinocyte responses to inflammatory stress and support its further investigation in OLP-associated epithelial injury.