AI Article Synopsis
- Oral leukoplakia (OLK) is a common oral condition that can lead to cancer, and the study investigates the role of the Prx1/PHB2 relationship in OLK progression through mitophagy (cellular process involving mitochondria).
- The research involved analyzing tissue samples and cell lines to assess biomarkers related to cell proliferation and aging, highlighting the increased expression of key proteins associated with OLK and oral squamous cell carcinoma (OSCC).
- Results indicate that Prx1 mutations influence the interaction with PHB2, affecting mitochondrial function and cell senescence, which suggests that Prx1Cys52 could be a promising target for clinical interventions in OLK.
Article Abstract
Background: Oral leukoplakia (OLK) is the most common oral potentially malignant disorder (OPMD), which can be malignantly transformed into oral squamous cell carcinoma (OSCC). Peroxiredoxin1(Prx1) has been predicted to bind to Prohibitin2 (PHB2), which confers to affect OLK progression; however, the mechanism of Prx1/PHB2 mediated mitophagy involved in OLK remains unclear.
Methods: This study aimed to explore the mechanism of the Prx1/PHB2 axis on senescence in OLK through mediating mitophagy. The positive rate of Ki67 and the expression of p21, p16, PHB2, and LC3 in human normal, OLK, and OSCC tissues were detected by immunohistochemical staining. The mitophagy and mitochondrial function changes were then analyzed in Prx1 knockdown and Prx1C52S mutations in dysplastic oral keratinocyte (DOK) cells treated with HO. In situ Proximity Ligation Assay combined with co-immunoprecipitation was used to detect the interaction between Prx1 and PHB2.
Results: Clinically, the positive rate of Ki67 progressively increased from normal to OLK, OLK with dysplasia, and OSCC. Higher p21, p16, PHB2, and LC3 expression levels were observed in OLK with dysplasia than in normal and OSCC tissues. In vitro, PHB2 and LC3II expression gradually increased with the degree of DOK cell senescence. Prx1/PHB2 regulated mitophagy and affected senescence in HO-induced DOK cells. Furthermore, Prx1C52S mutation specifically reduced interaction between Prx1 and PHB2. Prx1Cys52 is associated with mitochondrial reactive oxygen species (ROS) accumulated and cell cycle arrest.
Conclusion: Prx1Cys52 functions as a redox sensor that binds to PHB2 and regulates mitophagy in the senescence of OLK, suggesting its potential as a clinical target.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.prp.2024.155411 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Identification of high-risk oral leukoplakia (OLK) using combined Raman spectroscopic analysis of brush biopsy and saliva samples: A proof of concept study.
Spectrochim Acta A Mol Biomol Spectrosc
January 2025
Centre for Radiation and Environmental Science, FOCAS Research Institute, Technological University Dublin, City Campus, Dublin, Ireland; School of Physics, Clinical and Optometric Sciences, Technological University Dublin, City Campus, Dublin, Ireland.
The gold standard method of diagnosis of oral leukoplakia (OLK) is a tissue biopsy followed by histological examination. Raman spectroscopic studies of cytological brush biopsy and saliva samples have previously been shown to differentiate low (no and mild dysplasia) and high risk (moderate and severe dysplasia) OLKs, discriminant models of cellular samples achieving higher specificity, whereas those based on saliva samples achieved higher sensitivity. The current study combines the spectral data sets of cell and saliva samples in an attempt to improve the overall efficiency of the discriminating models.
View Article and Find Full Text PDFMetabolomic Profiling of Oral Potentially Malignant Disorders and Its Clinical Values.
Biomedicines
December 2024
Department of Oral and Maxillofacial Clinical Sciences, Faculty of Dentistry, Universiti Malaya, Kuala Lumpur 50603, Malaysia.
Oral potentially malignant disorders (OPMD) are a group of lesions carrying the risk of developing into cancer. The gold standard to predict which lesions are more likely to undergo malignant transformation is the presence of dysplasia histologically. However, not all dysplastic lesions progress, and non-dysplastic lesions may also undergo malignant transformation.
View Article and Find Full Text PDFAdhesive lipophilic gels delivering rapamycin prevent oral leukoplakia from malignant transformation.
Mater Today Bio
December 2024
State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, Med-X Center for Materials, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, PR China.
Article Synopsis
- Oral leukoplakia (OLK) is a potentially malignant disorder that can progress to oral squamous cell carcinoma (OSCC) with a transformation rate of about 9.8%, highlighting the need for early intervention.
- Rapamycin shows promise in preventing OLK from becoming cancerous due to its ability to penetrate the skin barrier, but effective delivery into the complex oral environment has been a challenge.
- A newly developed dual-function hydrogel system combining polyvinyl alcohol (PVA) and dioleoyl phosphatidylglycerol (DOPG) demonstrates strong adhesive properties and enhances the penetration of rapamycin, showing effectiveness in reducing malignant transformations in a mouse model.
Heat Shock Protein 70-2 is Overexpressed in Oral Leukoplakia and Oral Squamous Cell Carcinoma.
Int Dent J
November 2024
Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi, China. Electronic address:
Objective: The objective of this study was to assess the correlation between the expression of HSP70-2 and the development of oral potentially malignant disorders (OPMD) and oral squamous cell carcinoma (OSCC). Furthermore, the study evaluates the potential function of HSP70-2 in the pathogenesis of malignant diseases of the oral cavity.
Methods: Using immunohistochemistry, RT-qPCR, Western blot, indirect immunofluorescence, and flow cytometry, the expression of HSP70-2 mRNA and protein in OPMD and OSCC tissues and cells was investigated.
FGF6 inhibits oral squamous cell carcinoma progression by regulating PI3K/AKT and MAPK pathways.
Sci Rep
November 2024
Department of Oral Basic Medicine, The Affiliated Stomatological Hospital of Southwest Medical University, Luzhou, 646000, Sichuan, China.
To explore diagnostic and prognostic biomarkers in the progression of oral squamous cell carcinoma (OSCC) and to reveal their regulatory mechanisms in key pathways. A RayBiotech protein chip was used to screen differentially expressed serum proteins in OSCC, oral leukoplakia (OLK), and healthy participants. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were used to determine the pathways enriched by characteristic differential proteins.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!