Role of the Wnt signalling pathway in oral cancer | ||||
| Egyptian Dental Journal | ||||
| Article 1, Volume 69, Issue 2 - Serial Number 3, April 2023, Page 995-1005 PDF (4.6 MB) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/edj.2023.178343.2364 | ||||
 View on SCiNiTO | ||||
| Author | ||||
Hanaa abdelsamia  
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| Lecturer of Oral and Dental Pathology. Faculty of Dental Medicine, Al Azhar University (Girls Branch), Cairo, Egypt. | ||||
| Abstract | ||||
| The sixth most dangerous cancer worldwide is oral cancer. Pre-cancer disorders are often present in many patients before oral cancer develops. Several types of human cancer have been linked to abnormal activation of Wnt/β-catenin signaling, which is characterized by β-catenin translocation and overexpression of Wnt ligands. β-catenin interacts with the transcription factor during canonical Wnt/β-catenin signaling to activate downstream target genes such as Cyclin D1, which is primarily associated with cellular proliferation. This study aims to evaluate the role of β- catenin and Cyclin D1 in epithelial dysplasia and various stages of oral squamous cell carcinoma (OSCC) via the Wnt signaling pathway. For the present study, 5 cases of normal oral epithelial tissues, 10 cases of severe epithelial dysplasia, and 30 cases of various grades of OSCC (10 cases for each grade) were collected as paraffin-embedded blocks. All specimens were immunohistochemically stained for β-catenin and Cyclin D1 antibodies. β-catenin immunostaining showed the highest mean area percentage found in normal epithelial tissue, whereas the lowest values were recorded in poorly-differentiated OSCC, while Cyclin D1 immunostaining showed the lowest mean area percent was recorded in normal epithelial tissue, whereas the highest values were noted in poorly-differentiated OSCC. Conclusion: Aberrant cytoplasmic expression of β-catenin act as a co-factor, activating Cyclin D1 lead to high proliferative activity and invasion potential. Thus associations of both molecules has greater role in transformation from normal to dysplastic cells and increase their invasiveness to OSCC. | ||||
| Keywords | ||||
| Oral cancer; β-catenin; Wnt signaling pathway; Cyclin D1 | ||||
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