Affiliation:
1. KLE University’s VK Institute of Dental Sciences, Belgaum, Karnataka, India
2. AC Patil Memorial Medical College, Dhule, Maharashtra
3. KLE University’s JN Medical College, Belgaum, Karnataka, India
Abstract
Aims. Epithelial mesenchymal transition (EMT) is a crucial process for acquisition of malignant phenotype, aggressiveness, and metastatic capacity in neoplasms. It is characterized by loss of epithelial markers and gain of mesenchymal markers. Studies on EMT and its potential association with the histological grading are sparse in oral squamous cell carcinoma (OSCC). This study aims to evaluate the expression of EMT-associated proteins—E-cadherin, β-catenin, and N-cadherin—in different grades of OSCC. Methodology. In all, 60 cases of OSCC further subdivided into 20 cases each of well-, moderately, and poorly differentiated OSCCs were stained immunohistochemically with E-cadherin, β-catenin, and N-cadherin antibodies. The differences in the expression were evaluated using χ2 and Fisher exact tests, whereas Spearman’s correlation was used to analyze the correlation between the markers. Results. A reduced E-cadherin expression noted in 40% of the OSCCs was associated with reduced β-catenin expression in 66.6% of the cases and increase in the expression of mesenchymal N-cadherin seen in 80% of cases. This expression pattern demonstrated a significant association with histological grades. A membrane to cytoplasmic shift of E-cadherin (73.3%) and β-catenin (78.3%) increased with histological grade. A negative correlation was observed with the E-cadherin and N-cadherin localization, though it did not reach statistical significance. Conclusion. OSCC tissues had high levels of EMT phenotype as compared with the normal oral mucosa. This phenotype was characterized by reduced E-cadherin and β-catenin expression and overexpression of N-cadherin. Aberrant localization of the studied proteins was a hallmark for depicting EMT.
Subject
Pathology and Forensic Medicine,Surgery,Anatomy
Cited by
37 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献