Immunohistochemical expression of E-cadherin and Bcl-2 in oral squamous cell carcinoma.

Abstract

Background: The most frequent malignancy of the oral cavity is oral squamous cell carcinoma (OSCC), which accounts for up to 80-90% of all malignant neoplasms of the oral cavity. It results from the gradual accumulation of diverse genetic alterations. Alcohol use, tobacco use, betel quid chewing, human papillomavirus (HPV) and poor nutrition are significant risk factors for oral squamous cell carcinoma (OSCC). The cancer suppressor gene E-cadherin establishes a cutoff for Wnt-catenin signaling. Cell-cell adhesion is lost as a result of the Wnt signaling pathway being amplified when E-Cadherin expression is diminished. An antiapoptotic protein called B-cell lymphoma-2 (Bcl-2) interacts with and is controlled by P53. It is a component of the regulatory network that manages the cell cycle and triggers apoptosis.

Methods: A retrospective study was conducted on 60 formalin-fixed, paraffin-embedded tissue blocks, comprising 20 cases each of well-differentiated, moderately differentiated, and poorly differentiated oral squamous cell carcinoma (OSCC). Diagnosis was based on hematoxylin and eosin staining, with oral mucosa serving as the control.

Results: In increasing grades of OSCC, E-cadherin was downregulated and Bcl-2 was overexpressed; the difference was statistically significant.

Conclusion: The relationship between E-cadherin and Bcl-2 was shown to be inverse. Both predictive and therapeutic uses of the indicators are possible.