Affiliations 

  • 1 Centre for Preclinical Science Studies, Faculty of Dentistry, Universiti Teknologi MARA, Sungai Buloh Campus, Jalan Hospital, 47000, Sungai Buloh, Selangor, Malaysia
  • 2 Centre for Oral and Maxillofacial Diagnostic and Medicine, Faculty of Dentistry, Universiti Teknologi MARA, Sungai Buloh Campus, Jalan Hospital, 47000, Sungai Buloh, Selangor, Malaysia
  • 3 Department of Pathology, Faculty of Medicine, Universiti Teknologi MARA, Sungai Buloh Campus, Jalan Hospital, 47000, Sungai Buloh, Selangor, Malaysia
Saudi Dent J, 2021 Dec;33(8):813-818.
PMID: 34938020 DOI: 10.1016/j.sdentj.2021.08.002

Abstract

The Wnt signalling pathway involves in the pathogenesis of human diseases and one of the pathways that contribute to embryogenic development. Studies about the Wnt pathway have unfolded its regulation in many cancer cell mechanisms such as cell survival, migration, polarity, and cell multiplication. Moreover, the Wnt pathway has a significant role in cell fate determination and self-renewal in stem cells. Oral cancer shares significant concern among clinicians and researchers. However, there are only a few studies done on oral cancer and its correlation with the Wnt pathway. The expression of Wnt gene members in many malignancy diseases which included oral cancer has proven a high inverse correlation with malignancy diseases and malignancy progression. Metastasis which predominantly occurred through the lymphatic system has been the principal cause of mortality in oral cancer and affected to cancer stage, main tumour site, cancer cell differentiation and cancer cell adhesion potency. With intention of contributing to oral pathology and oral medicine research and knowledge advancement, particularly in the oral cancer area, this article presents current findings regarding the Wnt pathway and its multiple mechanisms associated with the treatment of oral carcinogenesis through Wnt pathway signalling.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.