SDHB reduction promotes oral lichen planus by impairing mitochondrial respiratory function
Hui Zhang1, Beiyun Xu1, Jin Liu1
1Department of Stomatology, Huashan Hospital, Fudan University, Shanghai, China.
Annals of Translational Medicine
|January 20, 2023
Summary
Reduced succinate dehydrogenase B (SDHB) expression in oral lichen planus (OLP) impairs mitochondrial function, potentially increasing oral cancer risk. Restoring SDHB levels may reverse these detrimental effects.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Oral lichen planus (OLP) is a chronic inflammatory condition with malignant transformation potential.
- Succinate dehydrogenase B (SDHB) is linked to oral squamous cell carcinoma (OSCC) carcinogenesis, but its role in OLP is unclear.
Purpose of the Study:
- To investigate the expression and function of SDHB in OLP.
- To elucidate the mechanism by which SDHB influences OLP pathogenesis and potential malignant transformation.
Main Methods:
- Immunohistochemistry (IHC), qRT-PCR, and Western Blot (WB) were used to assess SDHB expression in OLP tissues and cell models.
- Functional assays including ATP, ROS, mitochondrial membrane potential (MMP), and glucose uptake were performed to evaluate SDHB's role in mitochondrial injury and bioenergetics.
Main Results:
- SDHB mRNA and protein levels were significantly decreased in OLP patients, correlating with succinate accumulation.
- Decreased SDHB in OLP cell models enhanced HIF-1α activity, induced mitochondrial dysfunction, altered bioenergetics, and promoted cytokine release.
- SDHB overexpression reversed these pathological changes and modulated bioenergetic metabolism.
Conclusions:
- Reduced SDHB expression is a key factor in OLP development by impairing mitochondrial respiratory function.
- Targeting SDHB may offer a therapeutic strategy to mitigate OLP progression and reduce oral cancer risk.
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